Understanding the role of inflammation in the body at the molecular level could pave the way for a new generation of pharmaceuticals and treatments. Because inflammation accompanies nearly every illness and disease, the potential for new developments is enormous. Can I take a pill that helps reduce the inflammatory burden?

Too much inflammation in and of itself can kill by, for example, flooding the lungs with fluid or causing dehydration. Now we understand that inflammation can be both a cause and an effect, Iwasaki said. Obesity and diabetes are examples, she continued.

When people become overweight, their fat cells become bigger. Immune system cells called macrophages, whose job is to maintain homeostasis, sense something is wrong, and they deploy disease-fighting small proteins called cytokines against the cells, creating inflammation.

While the tipping point remains unclear—it appears to vary from person to person—the resulting inflammation can lead to diabetes and heart disease. Exactly how that happens requires further study, said Iwasaki.

Research indicates that an immune reaction to amyloid plaques in the brain may contribute to the dreaded illness. According to the model, macrophages interpret crystal-like plaques in the brain as foreign objects and begin secreting cytokines that attack them, which leads to inflammation and destruction of neurons culminating in dementia.

Ultimately, inflammation may also play a role in such behaviors as depression and suicide, she said. Hafler, an expert on MS, cites yet another example of the double duty performed by inflammatory cytokines. His lab compared spinal fluid from healthy medical students and patients with MS.

Unsurprisingly, the fluid from MS patients was inflamed—but so was that of the healthy medical students. They are also coming to believe that a healthy microbiome—the billions of bacteria in the gut that help us process food—may be key to avoiding that potentially disease-inducing inflammation.

The microbiome is exquisitely sensitive, Palm said. Changes in diet, or even something as seemingly benign as living with a dog, significantly alter the teeming microbial communities that populate our guts, he said. At the same time, the incidence of certain inflammatory illnesses and conditions—allergies, obesity, heart disease, diabetes—has exploded.

Is there a connection? He has already begun to establish potential causation in certain illnesses , specifically inflammatory bowel disease IBD.

He and his lab assistants have found that when microbiome material from an IBD sufferer is inserted into an otherwise healthy mouse, the mouse will develop a disease that looks similar to human IBD. While genetic factors may also be involved , these findings indicate that particular bacteria may trigger IBD in at least a subset of patients.

Jorge Galán, PhD, DVM , the Lucille P. The long-held view was that the inflammation resulting from Salmonella infection, which makes you sick, was caused by the immune system attacking the pathogen. Nutrients are scarce in the gut, Galán added.

In order to make those nutrients available, Salmonella and similar pathogens must induce inflammation. Salmonella meets this goal by injecting proteins that trigger inflammation , thereby producing the nutrients it needs to survive, Galán said.

Instead of killing the pathogen with a classic antibiotic, you can try to formulate a targeted drug that simply shuts off the microinjection device inducing the inflammation, he said.

Certainly the evolutionary process that leads to antibiotic resistance would be slowed significantly. The promise of a deeper understanding of inflammation and its roles in sickness and health is significant, potentially paving the way for individualized and less invasive treatments that work in harmony with the body, researchers say.

It may well boil down to learning how to turn inflammation from on to off. Skip to Main Content Information for About YSM. About YSM. YSM Administration. Department Chairs. YSM Executive Group. YSM Board of Permanent Officers. Faculty Advisory Council.

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Physician-Scientist Development Awards. Fund for Physician-Scientist Mentorship. Grant Library. Smoking, being sedentary, or eating a diet high in processed foods and refined carbohydrates can contribute to chronic inflammation. This ongoing inflammation increases the risk of many diseases—including heart disease, stroke, diabetes, cancer, and chronic obstructive pulmonary disease.

The signs of chronic inflammation are not as obvious as those of acute inflammation. No sharp twinge of pain as when you cut yourself, no swelling or redness will you see to alert you to a problem.

Chronic inflammation can be widespread or more localized to specific areas of the body. Some of the symptoms associated with chronic inflammation include:.

For additional advice about ways to reduce inflammation, check out Fighting Inflammation , a Special Health Report from Harvard Medical School.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles.

No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

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bacteria and compromise the survival of the organism. In contrast, too much inflammation, in the form of chronic inflammation, is associated with various diseases, such as hay fever , periodontal disease , atherosclerosis , and osteoarthritis. Inflammation can be classified as acute or chronic.

Acute inflammation is the initial response of the body to harmful stimuli, and is achieved by the increased movement of plasma and leukocytes in particular granulocytes from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system , the immune system , and various cells in the injured tissue.

Prolonged inflammation, known as chronic inflammation , leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells , and involves simultaneous destruction and healing of the tissue. Inflammation has also been classified as Type 1 and Type 2 based on the type of cytokines and helper T cells Th1 and Th2 involved.

The term inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response—the two components are considered together in discussion of infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction.

Inflammation , on the other hand, describes just the body's immunovascular response, regardless of cause. But, because of the two are often correlated , words ending in the suffix -itis which means inflammation are sometimes informally described as referring to infection: for example, the word urethritis strictly means only "urethral inflammation", but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

However, the inflammation—infection distinction is crucial in situations in pathology and medical diagnosis that involve inflammation that is not driven by microbial invasion, such as cases of atherosclerosis , trauma , ischemia , and autoimmune diseases including type III hypersensitivity.

Chemical: [5]. Acute inflammation occurs immediately upon injury, lasting only a few days. Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus.

In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases. The first four classical signs were described by Celsus c. Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings.

Loss of function has multiple causes. Acute inflammation of the lung usually as in response to pneumonia does not cause pain unless the inflammation involves the parietal pleura , which does have pain-sensitive nerve endings.

The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident macrophages , dendritic cells , histiocytes , Kupffer cells and mast cells.

These cells possess surface receptors known as pattern recognition receptors PRRs , which recognize i. PAMPs are compounds that are associated with various pathogens , but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related injury and cell damage.

At the onset of an infection, burn, or other injuries, these cells undergo activation one of the PRRs recognize a PAMP or DAMP and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes the redness rubor and increased heat calor.

Increased permeability of the blood vessels results in an exudation leakage of plasma proteins and fluid into the tissue edema , which manifests itself as swelling tumor. Some of the released mediators such as bradykinin increase the sensitivity to pain hyperalgesia , dolor.

The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils and macrophages , to flow out of the blood vessels extravasation and into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.

In addition to cell-derived mediators, several acellular biochemical cascade systems—consisting of preformed plasma proteins—act in parallel to initiate and propagate the inflammatory response.

These include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated by necrosis e. Acute inflammation may be regarded as the first line of defense against injury.

Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed. Chronic inflammation is inflammation that lasts for months or years.

Common signs and symptoms that develop during chronic inflammation are: [9]. As defined, acute inflammation is an immunovascular response to inflammatory stimuli, which can include infection or trauma.

Upon contact with PAMPs, tissue macrophages and mastocytes release vasoactive amines such as histamine and serotonin , as well as eicosanoids such as prostaglandin E2 and leukotriene B4 to remodel the local vasculature. The increased collection of fluid into the tissue causes it to swell edema.

If the inflammatory stimulus is a lacerating wound, exuded platelets , coagulants , plasmin and kinins can clot the wounded area using vitamin K-dependent mechanisms [24] and provide haemostasis in the first instance. These clotting mediators also provide a structural staging framework at the inflammatory tissue site in the form of a fibrin lattice — as would construction scaffolding at a construction site — for the purpose of aiding phagocytic debridement and wound repair later on.

Some of the exuded tissue fluid is also funneled by lymphatics to the regional lymph nodes, flushing bacteria along to start the recognition and attack phase of the adaptive immune system. Acute inflammation is characterized by marked vascular changes, including vasodilation , increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators.

Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood — a condition characterized by enlarged vessels packed with cells.

Stasis allows leukocytes to marginate move along the endothelium , a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel. The cellular component involves leukocytes , which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation.

Others release enzymatic granules that damage pathogenic invaders. Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. In general, acute inflammation is mediated by granulocytes , whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.

Various leukocytes , particularly neutrophils, are critically involved in the initiation and maintenance of inflammation. These cells must be able to move to the site of injury from their usual location in the blood, therefore mechanisms exist to recruit and direct leukocytes to the appropriate place.

The process of leukocyte movement from the blood to the tissues through the blood vessels is known as extravasation and can be broadly divided up into a number of steps:.

Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue. Phagocytes express cell-surface endocytic pattern recognition receptors PRRs that have affinity and efficacy against non-specific microbe-associated molecular patterns PAMPs.

Most PAMPs that bind to endocytic PRRs and initiate phagocytosis are cell wall components, including complex carbohydrates such as mannans and β- glucans , lipopolysaccharides LPS , peptidoglycans , and surface proteins. Endocytic PRRs on phagocytes reflect these molecular patterns, with C-type lectin receptors binding to mannans and β-glucans, and scavenger receptors binding to LPS.

Upon endocytic PRR binding, actin - myosin cytoskeletal rearrangement adjacent to the plasma membrane occurs in a way that endocytoses the plasma membrane containing the PRR-PAMP complex, and the microbe. Phosphatidylinositol and Vps34 - Vps15 - Beclin1 signalling pathways have been implicated to traffic the endocytosed phagosome to intracellular lysosomes , where fusion of the phagosome and the lysosome produces a phagolysosome.

The reactive oxygen species , superoxides and hypochlorite bleach within the phagolysosomes then kill microbes inside the phagocyte. Phagocytic efficacy can be enhanced by opsonization. Plasma derived complement C3b and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens.

As well as endocytic PRRs, phagocytes also express opsonin receptors Fc receptor and complement receptor 1 CR1 , which bind to antibodies and C3b, respectively. The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the lysosomal elimination of the infective agent.

Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved.

Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, as demonstrated in both allergic reactions and some myopathies , with many immune system disorders resulting in abnormal inflammation.

Non-immune diseases with causal origins in inflammatory processes include cancer, atherosclerosis , and ischemic heart disease. Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response.

Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of atherosclerosis from initiation through progression and, ultimately, the thrombotic complications from it.

These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage.

In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein , prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors.

Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, the anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels.

These new insights on inflammation contribute to the etiology of atherosclerosis, and the practical clinical applications in risk stratification and the targeting of therapy for atherosclerosis.

An allergic reaction, formally known as type 1 hypersensitivity , is the result of an inappropriate immune response triggering inflammation, vasodilation, and nerve irritation.

A common example is hay fever , which is caused by a hypersensitive response by mast cells to allergens. Pre-sensitised mast cells respond by degranulating , releasing vasoactive chemicals such as histamine.

These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes.

Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis , and include dermatomyositis , polymyositis , and inclusion body myositis.

Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte functionality often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.

In addition, diseases affecting the bone marrow may result in abnormal or few leukocytes. Certain drugs or exogenous chemical compounds are known to affect inflammation.

Vitamin A deficiency, for example, causes an increase in inflammatory responses, [30] and anti-inflammatory drugs work specifically by inhibiting the enzymes that produce inflammatory eicosanoids.

Additionally, certain illicit drugs such as cocaine and ecstasy may exert some of their detrimental effects by activating transcription factors intimately involved with inflammation e. Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration.

On the other hand, due to the modular nature of many steroid hormone receptors, this interaction may offer ways to interfere with cancer progression, through targeting of a specific protein domain in a specific cell type.

Such an approach may limit side effects that are unrelated to the tumor of interest, and may help preserve vital homeostatic functions and developmental processes in the organism.

According to a review of , recent data suggests that cancer-related inflammation CRI may lead to accumulation of random genetic alterations in cancer cells. In , Rudolf Virchow hypothesized that the origin of cancer was at sites of chronic inflammation. Inflammation also causes DNA damages due to the induction of reactive oxygen species ROS by various intracellular inflammatory mediators.

ROS and RNS are normally produced by these cells to fight infection. A normal cell may undergo carcinogenesis to become a cancer cell if it is frequently subjected to DNA damage during long periods of chronic inflammation.

DNA damages may cause genetic mutations due to inaccurate repair. In addition, mistakes in the DNA repair process may cause epigenetic alterations. Genome-wide analyses of human cancer tissues reveal that a single typical cancer cell may possess roughly mutations in coding regions , 10—20 of which are "driver mutations" that contribute to cancer development.

Typically, several hundreds to thousands of genes are methylated in a cancer cell see DNA methylation in cancer. Sites of oxidative damage in chromatin can recruit complexes that contain DNA methyltransferases DNMTs , a histone deacetylase SIRT1 , and a histone methyltransferase EZH2 , and thus induce DNA methylation.

DNA repair genes, in particular, are frequently inactivated by methylation in various cancers see hypermethylation of DNA repair genes in cancer.

A report [49] evaluated the relative importance of mutations and epigenetic alterations in progression to two different types of cancer. This report showed that epigenetic alterations were much more important than mutations in generating gastric cancers associated with inflammation.

It has long been recognized that infection with HIV is characterized not only by development of profound immunodeficiency but also by sustained inflammation and immune activation.

Animal studies also support the relationship between immune activation and progressive cellular immune deficiency: SIV sm infection of its natural nonhuman primate hosts, the sooty mangabey , causes high-level viral replication but limited evidence of disease.

In sharp contrast, experimental SIV sm infection of rhesus macaque produces immune activation and AIDS-like disease with many parallels to human HIV infection.

Delineating how CD4 T cells are depleted and how chronic inflammation and immune activation are induced lies at the heart of understanding HIV pathogenesis—one of the top priorities for HIV research by the Office of AIDS Research, National Institutes of Health.

Recent studies demonstrated that caspase-1 -mediated pyroptosis , a highly inflammatory form of programmed cell death, drives CD4 T-cell depletion and inflammation by HIV.

Pyroptosis appears to create a pathogenic vicious cycle in which dying CD4 T cells and other immune cells including macrophages and neutrophils release inflammatory signals that recruit more cells into the infected lymphoid tissues to die.

The feed-forward nature of this inflammatory response produces chronic inflammation and tissue injury. In this regard, pyroptosis of CD4 T cells and secretion of pro-inflammatory cytokines such as IL-1β and IL can be blocked in HIV-infected human lymphoid tissues by addition of the caspase-1 inhibitor VX, [59] which has already proven to be safe and well tolerated in phase II human clinical trials.

Such agents would almost certainly be used in combination with ART. By promoting "tolerance" of the virus instead of suppressing its replication, VX or related drugs may mimic the evolutionary solutions occurring in multiple monkey hosts e.

the sooty mangabey infected with species-specific lentiviruses that have led to a lack of disease, no decline in CD4 T-cell counts, and no chronic inflammation. The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.

Resolution of inflammation occurs by different mechanisms in different tissues. Mechanisms that serve to terminate inflammation include: [12] [64]. Acute inflammation normally resolves by mechanisms that have remained somewhat elusive.

Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid —derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence.

Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids , of resolvins and protectins , which critically shorten the period of neutrophil infiltration by initiating apoptosis.

As a consequence, apoptotic neutrophils undergo phagocytosis by macrophages , leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-β1.

The anti-inflammatory program ends with the departure of macrophages through the lymphatics. There is evidence for a link between inflammation and depression. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression. Levels of cytokines tend to increase sharply during the depressive episodes of people with bipolar disorder and drop off during remission.

There is evidence for a link between inflammation and delirium based on the results of a recent longitudinal study investigating CRP in COVID patients. An infectious organism can escape the confines of the immediate tissue via the circulatory system or lymphatic system , where it may spread to other parts of the body.

If an organism is not contained by the actions of acute inflammation, it may gain access to the lymphatic system via nearby lymph vessels. An infection of the lymph vessels is known as lymphangitis , and infection of a lymph node is known as lymphadenitis. When lymph nodes cannot destroy all pathogens, the infection spreads further.

A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system. When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed.

When it is due to infection , the term sepsis is applied, with the terms bacteremia being applied specifically for bacterial sepsis and viremia specifically to viral sepsis. Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death.

Inflammation also is characterized by high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial; however, in chronic inflammation, they can contribute to amyloidosis.

With the discovery of interleukins IL , the concept of systemic inflammation developed. Although the processes involved are identical to tissue inflammation, systemic inflammation is not confined to a particular tissue but involves the endothelium and other organ systems.

Chronic inflammation is widely observed in obesity. Low-grade chronic inflammation is characterized by a two- to threefold increase in the systemic concentrations of cytokines such as TNF-α, IL-6, and CRP. Loss of white adipose tissue reduces levels of inflammation markers.

C-reactive protein CRP is generated at a higher level in obese people, and may increase the risk for cardiovascular diseases.

The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred—and the injurious agent that is causing it. Here are the possible outcomes to inflammation: [12]. Inflammation is usually indicated by adding the suffix " itis ", as shown below.

However, some conditions, such as asthma and pneumonia , do not follow this convention. More examples are available at List of types of inflammation. Contents move to sidebar hide. Article Talk. Read Edit View history. Tools Tools. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item.

Download as PDF Printable version. In other projects. Wikimedia Commons. Physical effects resulting from activation of the immune system. This article needs more reliable medical references for verification or relies too heavily on primary sources.

Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed.

Find sources: "Inflammation" — news · newspapers · books · scholar · JSTOR March Medical condition. Physical: Burns [5] Frostbite Physical injury , blunt or penetrating [6] Foreign bodies, including splinters , dirt and debris Trauma [5] Ionizing radiation Biological: Infection by pathogens [5] Immune reactions due to hypersensitivity Stress Chemical: [5] Chemical irritants Toxins Alcohol Psychological: Excitement [7].

This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. April Learn how and when to remove this template message. See also: List of inflammatory disorders and List of types of inflammation by location.

This section needs more reliable medical references for verification or relies too heavily on primary sources. Please review the contents of the section and add the appropriate references if you can. Find sources: "Inflammation" — news · newspapers · books · scholar · JSTOR April Main article: Chronic inflammation.

Main article: Leukocyte extravasation. Main article: Phagocyte. Acne vulgaris Asthma Autoimmune diseases Autoinflammatory diseases Celiac disease Chronic prostatitis Colitis Diverticulitis Familial Mediterranean Fever Glomerulonephritis Hidradenitis suppurativa Hypersensitivities Inflammatory bowel diseases Interstitial cystitis Lichen planus Mast Cell Activation Syndrome Mastocytosis Otitis Pelvic inflammatory disease Peripheral ulcerative keratitis Pneumonia Reperfusion injury Rheumatic fever Rheumatoid arthritis Rhinitis Sarcoidosis Transplant rejection Vasculitis.

Main article: Atherosclerosis. Short half-life of inflammatory mediators in vivo. Production and release of transforming growth factor TGF beta from macrophages [65] [66] [67] Production and release of interleukin 10 IL [68] Production of anti-inflammatory specialized proresolving mediators , i.

lipoxins , resolvins , maresins , and neuroprotectins [69] [70] Downregulation of pro-inflammatory molecules, such as leukotrienes. Upregulation of anti-inflammatory molecules such as the interleukin 1 receptor antagonist or the soluble tumor necrosis factor receptor TNFR Apoptosis of pro-inflammatory cells [71] Desensitization of receptors.

Increased survival of cells in regions of inflammation due to their interaction with the extracellular matrix ECM [72] [73] Downregulation of receptor activity by high concentrations of ligands Cleavage of chemokines by matrix metalloproteinases MMPs might lead to production of anti-inflammatory factors.

Fever Increased blood pressure Decreased sweating Malaise Loss of appetite Somnolence. IL-8 Interleukin-8 IL Interleukin [89] [90] TNF-α Tumor necrosis factor-alpha [89] [90] CRP C-reactive protein [89] [90] Insulin [89] [90] Blood glucose [89] [90] Leptin [89] [90]. Acute infective meningitis.

Anaphylatoxin Anti-inflammatories Essential fatty acid interactions Healing Inflammaging Inflammatory cytokine Inflammatory reflex Interleukin Lipoxin Neurogenic inflammation Substance P Stress biology Endothelial Cell Tropism.

Clinical and Experimental Immunology. doi : PMC PMID January Impact Journals, LLC. S2CID In Saunders Elsevier ed. Basic Immunology. Functions and disorders of the immune system 3rd ed. After sensing the toxins, bacteria and physical damage from the sting, the immune system deploys various types of immune cells to the site of the sting.

These include T cells, B cells, macrophages and neutrophils , among other cells. The B cells produce antibodies. Those antibodies can kill any bacteria in the wound and neutralize toxins from the sting. Macrophages and neutrophils engulf bacteria and destroy them.

Additionally, these immune cells produce hundreds of types of molecules called cytokines — otherwise known as mediators — that help fight threats and repair harm to the body. But just like in a military attack, inflammation comes with collateral damage.

The mediators that help kill bacteria also kill some healthy cells. Other similar mediating molecules cause blood vessels to leak, leading to accumulation of fluid and influx of more immune cells.

This collateral damage is the reason you develop swelling, redness and pain around a bee sting or after getting a flu shot.

Once the immune system clears an infection or foreign invader — whether the toxin in a bee sting or a chemical from the environment — different parts of the inflammatory response take over and help repair the damaged tissue. After a few days, your body will neutralize the poison from the sting, eliminate any bacteria that got inside and heal any tissue that was harmed.

Inflammation is a double-edged sword. It is critical for fighting infections and repairing damaged tissue, but when inflammation occurs for the wrong reasons or becomes chronic , the damage it causes can be harmful. Allergies , for example, develop when the immune system mistakenly recognizes innocuous substances — like peanuts or pollen — as dangerous.

Chronic inflammation damages tissues over time and can lead to many noninfectious clinical disorders , including cardiovascular diseases, neurodegenerative disorders, obesity, diabetes and some types of cancers. This self-targeted inflammation is what causes the symptoms of autoimmune diseases such as lupus and arthritis.

Another cause of chronic inflammation that researchers like us are currently studying is defects in the mechanisms that curtail inflammation after the body clears an infection. While inflammation mostly plays out at a cellular level in the body, it is far from a simple mechanism that happens in isolation.

Stress, diet and nutrition, as well as genetic and environmental factors, have all been shown to regulate inflammation in some way. There is still a lot to be learned about what leads to harmful forms of inflammation, but a healthy diet and avoiding stress can go a long way toward helping maintain the delicate balance between a strong immune response and harmful chronic inflammation.

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