Exercise, Inflammation, and Respiratory Infection
James M. Rippe in Lifestyle Medicine, 2019
Acute inflammation is a normal response of the immune system to infection and trauma. Intense and prolonged exercise similar to marathon race competition causes large but transient increases in total white blood cells (WBC) and a variety of cytokines including interleukin-6 (IL-6), IL-8, IL-10, IL-1 receptor antagonist (IL-1ra), granulocyte colony stimulating factor (GCSF), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1β), tumor necrosis factor-alpha (TNF-α), and macrophage migration inhibitory factor (MIF).2–4 C-reactive protein (CRP) is also elevated following heavy exertion, but the increase is delayed in comparison to most cytokines. Despite regular increases in these inflammation biomarkers during each intense exercise bout, endurance athletes have lower levels when measured during rest in contrast to overweight and unfit adults. For example, mean CRP levels in long-distance runners (rested state) typically fall below 0.5 mg/L in comparison to 4.0 mg/L and higher in obese, postmenopausal women.3,5
Inflammation
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Acute inflammation is caused by the direct action of irritants (bacteria, chemicals, physical damage, irradiation, and many other causes), and the subsequent attempt by the body or tissue to remove the irritant and restore the homeostasis.394 The first requisite for healing is the complete elimination of the harmful chemical or physical agent, or destruction of bacteria. Neither an inflammatory lesion nor a wound can heal if it still contains the corrosive chemical, a foreign body, or if it is infected. Dead fragments of tissue are removed through degradation by macrophages or by proteolysis. When this step has been accomplished, the process of healing can start, followed by sequential steps of repair. We use the word repair contemplating the fact that in this sense the human body has no replacement parts. If part of the kidney or any other organ is destroyed by inflammation, or another pathological process, the injured tissue is not replaced by new kidney tissue, but by scar tissue. With advancing age, degrading tissues can merely be replaced by scar tissue, which consists of strong and densely layered connective tissue fibers. Thus, connective tissue cannot substitute the original organ in the functional sense, and its composition reflects the change from tissues which possess diverse metabolic function and serve particular roles (Table 1).
Cancer
Sally Robinson in Priorities for Health Promotion and Public Health, 2021
Like atherosclerosis and cardiovascular disease, obesity and type 2 diabetes, cancer is often described as a chronic low-grade inflammatory disease. Acute inflammation occurs when we sustain an injury. Blood vessels dilate, blood flow increases and white blood cells cluster around the wound to alert cytokines, activate the immune system and support healing. If the body exhibits persistent inflammation at a low level and ‘doesn’t switch off’, it causes damage and disease. Low-grade inflammation may be triggered by internal and external threats, and these include age, excess body fat, a diet rich in saturated fat, trans fat and sugar, tobacco smoking and stress (Pahwa et al., 2020). The causes of cancer can be divided into the non-modifiable risk factors that we can’t change, and the modifiable ones that we can. Many may initially prompt low-grade inflammation which, in turn, may encourage cancer.
Dietary Fatty Acids and Other Nutrients in Relation to Inflammation and Particularly to Oral Mucosa Inflammation. A Literature Review
Published in Nutrition and Cancer, 2019
Evangelina Costantino, Adriana Beatriz Actis
The inflammation may be acute or chronic. The first is characterized by the movement of serum proteins and leukocytes from blood to extravascular tissue with an initial recruitment of neutrophils, followed by monocytes that differentiate into macrophages (12). These initial events of vascular permeability and leukocyte infiltration are regulated by lipid mediators such as prostaglandins (PGs), leukotrienes (LTs), cytokines, and chemokines (13–15). Acute inflammation is automatically finished by endogenous antiinflammatory and proresolving mediators such as resolvins, lipoxins, protectin, and maresin, biosynthesized from n-3 FAs (13,16–18). They stop the leukocyte infiltration, reverse vasodilation, and vascular permeability and promote the elimination of inflammatory cells, tissue exudate and debris, thereby restoring homeostasis (13,19). However, if timely resolution fails the inflammation persists and may progress to a chronic condition (20,21) which is a prolonged, dysregulatory, and maladaptive response that involves persistent active inflammation, tissue destruction, and failed attempts at tissue repair (22).
Relationship between obesity and iron deficiency anemia: is there a role of hepcidin?
Published in Hematology, 2018
Ertan sal, Idil Yenicesu, Nurullah Celik, Hatice Pasaoglu, Bulent Celik, Ozge Tugce Pasaoglu, Zühre Kaya, Ulker Kocak, Orhun Camurdan, Aysun Bideci, Peyami Cinaz
Serum ferritin, accepted to be a positive acute-phase protein, may be markedly elevated during states of inflammation, most probably due to elevated cytokine levels [22]. Acute inflammation may be caused by infection or injury, whereas chronic inflammation may result from metabolic disturbances. Both types of inflammation can affect the iron homeostasis by affecting the regulation and synthesis of certain hepatic acute-phase proteins, such as ferritin, transferrin, haptoglobin and hepcidin. These acute-phase proteins, once induced by the acute-phase response, may affect the distribution of iron to cells throughout the body [23]. As a result, the levels of most iron indicators will be directly affected by inflammation [24]. In addition, inflammation may affect iron balance negatively by decreasing both food intake and intestinal absorption [25].
The effect of red-to-near-infrared (R/NIR) irradiation on inflammatory processes
Published in International Journal of Radiation Biology, 2019
Tomasz Walski, Krystyna Dąbrowska, Anna Drohomirecka, Natalia Jędruchniewicz, Natalia Trochanowska-Pauk, Wojciech Witkiewicz, Małgorzata Komorowska
The wide range of applications that this radiation may have raises questions on the effects that R/NIR exerts on the immune system—specifically, the effects of R/NIR on immune cells that are effectors of the immune response and that mediate inflammation. Inflammation is a part of the body response to pathogens, irritants, trauma, and other harmful factors. The function of inflammation is to improve elimination of these harmful factors, also clearing out damaged cells and tissues. Typical signs of inflammation are heat, redness, pain, swelling, and loss of function. In spite of its important function in protection of a system from pathogen invasion or other harmful occurrences, prolonged inflammation may have a devastating effect on the system itself. This includes tissue damage and organ dysfunctions. Thus, control of inflammation can be a key step in many therapeutic strategies (Cotran et al. 1998; Ferrero-Miliani et al. 2007; Eming et al. 2007).
Related Knowledge Centers
- Adaptive Immune System
- Allergic Rhinitis
- Innate Immune System
- Necrosis
- White Blood Cell
- Blood Vessel
- Pathogen
- Irritation
- Signs & Symptoms
- Functio Laesa