Inflammation *

Inflammation (from Latin: inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

The five classical signs of inflammation are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa).[1] Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body.

Inflammation can be classified as either 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 (especially 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 within 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 is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

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 when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body’s immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to 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.

Inflammation and Cancer

Cancer cells can arise from tissue irritation, infections, and inflammation. One sarcoma we witnessed surfaced on a leg that had been traumatized with a baseball. When the quality of the blood and the strength of the immune system are not holistically maintained, then yes, irritation and inflammation can spur the production of cancer cells.

In fact,  inflammatory cells such as neutrophils can assist tumor cells to multiply and spread. Tumors have been likened to “wounds that won’t heal.”

Cells in a tumor act territorially, producing substances that attract nutrients and support structures to advance their survival. Among these molecules are chemokines, which draw neutrophils to a tumor. In turn, cancer cells can travel more easily through the body by hijacking a ride on the adhesion molecules that help propel the movement of the neutrophils.

As in wound healing, neutrophils, macrophages, lymphocytes, monocytes, and other white blood cells produce tissue-remodeling ingredients. These molecules spur the continued growth of cancer cells. On-site production of growth factors stimulates blood vessels to grow, to nourish the tumor and perpetuate the cycle.

Melanoma for example is thought to be caused in part by uncontrolled inflammation of the skin. A growing body of evidence supports a link between infection, inflammation, and many types of cancers. (Source)


Among other biological processes, infections also spur inflammation, if only to better subdue the infecting agent. (See File).  Among the cancers that are known to be associated with infection are certain types of lung, colon, pancreatic, and bladder tumors. Chronic infection with the hepatitis C virus is also a significant risk factor for liver cancer, and chronic infection with the ulcer-causing microorganism Helicobacter pylori is the world’s leading cause of stomach cancer.

Ectopic Endometrial cells are equally inflammatory. Up to 50 percent of women who suffer from this disease

In recent years, scientists have unveiled another link between inflammation and cancer. Medicines that block inflammation, such as aspirin, Tylenol and other so-called non-steroidal anti-inflammatory drugs (NSAIDs), have been shown to prevent certain kinds of colon, lung, mouth, and stomach cancers.

Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration.[3] Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis.[4] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.[5]Molecular intersection between receptors of steroid hormones, which have important effects on cellular development, and transcription factors that play key roles in inflammation, such as NF-κB, may mediate some of the most critical effects of inflammatory stimuli on cancer cells.[6] This capacity of a mediator of inflammation to influence the effects of steroid hormones in cells, is very likely to affect carcinogenesis on the one hand; 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 2009, recent data suggests that cancer-related inflammation (CRI) may lead to accumulation of random genetic alterations in cancer cells.[7]

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Cancer Lett. 2008 Aug 28;267(2):262-70. doi: 10.1016/j.canlet.2008.03.060. Epub 2008 May 23.

Inflammation and cancer: the oncogene-driven connection.

Borrello MG1, Degl’Innocenti D, Pierotti MA.

Author information


Inflammation has long been suspected to contribute to tumor growth. However, the concept that oncogenes, known for decades as responsible for cell neoplastic transformation, build up an inflammatory pro-tumorigenic microenvironment is emerging only in the last few years. The well known oncogenes RAS and MYC have been causally linked to tumor angiogenesis through different ways. Moreover, in thyroid tumors, where many of the genetic tumor-initiating events have been identified, the oncogenes driving tumorigenesis were proved able to induce an inflammatory program. This minireview will focus on growing evidence implicating the role of intrinsic, oncogene-driven pathways leading to pro-tumoral inflammation.

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  1. ^ Ferrero-Miliani L, Nielsen OH, Andersen PS, Girardin SE; Nielsen; Andersen; Girardin (February 2007). “Chronic inflammation: importance of NOD2 and NALP3 in interleukin-1beta generation”. Clin. Exp. Immunol. 147 (2): 061127015327006––. doi:10.1111/j.1365-2249.2006.03261.x. PMC 1810472
  2. ^ Abbas A.B.; Lichtman A.H. (2009). “Ch.2 Innate Immunity”. In Saunders (Elsevier). Basic Immunology. Functions and disorders of the immune system (3rd ed.). ISBN 978-1-4160-4688-2.
  3. ^ Montiel-Duarte, C.; Ansorena, E.; López-Zabalza, M. J.; Cenarruzabeitia, E.; Iraburu, M. J. (2004). “Role of reactive oxygen species, glutathione and NF-κB in apoptosis induced by 3,4-methylenedioxymethamphetamine (“Ecstasy”) on hepatic stellate cells”. Biochem Pharmacol. 67 (6): 1025–33. doi:10.1016/j.bcp.2003.10.020
  4. ^ Hendrik Ungefroren; Susanne Sebens; Daniel Seidl; Hendrik Lehnert; Ralf Haas (2011). “Interaction of tumor cells with the microenvironment”. Cell Communication and Signaling. 9 (18). doi:10.1186/1478-811X-9-18. PMC 3180438
  5. ^ Coussens, L. M.; Werb, Z. (2002). “Inflammation and cancer”. Nature. 420(6917): 860–7. Bibcode:2002Natur.420..860C. doi:10.1038/nature01322. PMC 2803035
  6. ^ Gunn, L; Ding, C; Liu, M; Ma, Y; Qi, C; Cai, Y; Hu, X; Aggarwal, D; Zhang, HG; Yan, J (Sep 15, 2012). “Opposing roles for complement component C5a in tumor progression and the tumor microenvironment”. Journal of Immunology. 189 (6): 2985–94. doi:10.4049/jimmunol.1200846. PMC 3436956.
  7. ^ Copland, JA; Sheffield-Moore, M; Koldzic-Zivanovic, N; Gentry, S; Lamprou, G; Tzortzatou-Stathopoulou, F; Zoumpourlis, V; Urban, RJ; Vlahopoulos, SA (Jun 2009). “Sex steroid receptors in skeletal differentiation and epithelial neoplasia: is tissue-specific intervention possible?”. BioEssays. 31 (6): 629–41. doi:10.1002/bies.200800138
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