Diet-induced obesity, exogenous leptin-, and MADB106 tumor cell challenge affect tissue leukocyte distribution and serum levels of cytokines in F344 rats

Behrendt, Patrick; Buchenauer, Tobias; Horn, Rüdiger; Brabant, Georg; Jacobs, Roland; Bode, Felix J; Stephan, Michael; Nave, Heike

doi:10.1007/s12020-010-9358-9

Cited by 5 publications

(5 citation statements)

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“…Several studies have shown inconsistent outcomes in terms of increasing or decreasing NK cell numbers. These discrepancies could be correlated with strain/species-dependent of the rodent models and their metabolic attributes or differences in the development, degradation, or migration of the NK cells (109)(110)(111). Compartmental NK cell distribution has also been studied along with the discrepancies mentioned above.…”

Section: Nk Cells In Obesity and Oamentioning

confidence: 99%

Obesity, Inflammation, and Immune System in Osteoarthritis

et al. 2022

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Obesity remains the most important risk factor for the incidence and progression of osteoarthritis (OA). The leading cause of OA was believed to be overloading the joints due to excess weight which in turn leads to the destruction of articular cartilage. However, recent studies have proved otherwise, various other factors like adipose deposition, insulin resistance, and especially the improper coordination of innate and adaptive immune responses may lead to the initiation and progression of obesity-associated OA. It is becoming increasingly evident that multiple inflammatory cells are recruited into the synovial joint that serves an important role in pathological changes in the synovial joint. Polarization of macrophages and macrophage-produced mediators are extensively studied and linked to the inflammatory and destructive responses in the OA synovium and cartilage. However, the role of other major innate immune cells such as neutrophils, eosinophils, and dendritic cells in the pathogenesis of OA has not been fully evaluated. Although cells of the adaptive immune system contribute to the pathogenesis of obesity-induced OA is still under exploration, a quantity of literature indicates OA synovium has an enriched population of T cells and B cells compared with healthy control. The interplay between a variety of immune cells and other cells that reside in the articular joints may constitute a vicious cycle, leading to pathological changes of the articular joint in obese individuals. This review addresses obesity and the role of all the immune cells that are involved in OA and summarised animal studies and human trials and knowledge gaps between the studies have been highlighted. The review also touches base on the interventions currently in clinical trials, different stages of the testing, and their shortcomings are also discussed to understand the future direction which could help in understanding the multifactorial aspects of OA where inflammation has a significant function.

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Section: Nk Cells In Obesity and Oamentioning

confidence: 99%

Obesity, Inflammation, and Immune System in Osteoarthritis

et al. 2022

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“…Data exist about differences in NK cell numbers in peripheral blood and organs, although the results are conflicting. Numerous studies demonstrated a decrease of the NK cell amount in blood as well as in spleen, lung, and liver of obese rodents (93,98,131,(140)(141)(142)(143). In contrast, other reports exist showing either no changes or an increase of the NK cell number in blood and different tissues of obese individuals (75,93,97,131,132,136,138,142).…”

Section: The Impact Of Systemic Obesity On Nk Cells In Animal Studiesmentioning

confidence: 99%

“…These discrepancies may be explained by species-or strain-dependent metabolic characteristics or by differences in developmental, degradation, or migration status of NK cells. In addition, compartment-specific NK cell distribution had been described, with an increased NK cell number in blood and spleen, but a decreased amount in the liver tissue of obese rats compared to their lean littermates (142). Moreover, heterogeneous methods of measurement may have led to different results.…”

Section: The Impact Of Systemic Obesity On Nk Cells In Animal Studiesmentioning

confidence: 99%

Obesity-Associated Alterations of Natural Killer Cells and Immunosurveillance of Cancer

et al. 2020

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Obesity is accompanied by a systemic chronic low-grade inflammation as well as dysfunctions of several innate and adaptive immune cells. Recent findings emphasize an impaired functionality and phenotype of natural killer (NK) cells under obese conditions. This review provides a detailed overview on research related to overweight and obesity with a particular focus on NK cells. We discuss obesity-associated alterations in subsets, distribution, phenotype, cytotoxicity, cytokine secretion, and signaling cascades of NK cells investigated in vitro as well as in animal and human studies. In addition, we provide recent insights into the effects of physical activity and obesity-associated nutritional factors as well as the reduction of body weight and fat mass on NK cell functions of obese individuals. Finally, we highlight the impact of impaired NK cell physiology on obesity-associated diseases, focusing on the elevated susceptibility for viral infections and increased risk for cancer development and impaired treatment response.NK cells are large granular lymphocytes that mediate rapid innate immunity against viruses, bacteria, parasites, and tumor cells without prior sensitization. NK cells primarily develop and mature in the bone marrow, migrate through the bloodstream, and seed into secondary lymphoid organs, like thymus, spleen, and lymph nodes as well as in other peripheral tissues, like lung, liver, kidney, uterus, and the gastrointestinal tract (23). In blood, NK cells represent 1-6% of all leukocytes and comprise up to 15% of human peripheral blood mononuclear cells (PBMCs). Human NK cells have been defined by the expression of adhesion molecule CD56 and by the absence of the T cell marker CD3. Based on their expression level of CD56 and the Fcγ receptor CD16, NK cells are subdivided into different subpopulations. The two major and classically defined subsets are the CD56 dim CD16 bright NK cells and the CD56 bright CD16 dim/neg NK cells. CD56 dim CD16 bright NK cells represent about 90% of all NK cells and are predominantly found in peripheral blood (24). They are mostly responsible for cytotoxic activity and target cell killing but are also a source of pro-inflammatory Abbreviations: ACM, adipocyte-conditioned media; Adamts3, a disintegrin-like and metallopeptidase with thrombospondin type 1 motif, 3; AdipoR, adiponectin receptor; Anxa8, annexin A8; AT, adipose tissue; Bax, Bcl-2-associated X protein; Bcl, B-cell lymphoma; BMI, body mass index; CCR, CC chemokine receptor; Csf1r, colony stimulating factor 1 receptor; CX3CR1, C-X3-C-motif chemokine receptor 1; DNAM-1, DNAX accessory molecule-1; ESR, estrogen receptor; FasL, Fas ligand; IFN-γ, interferon; GM-CSF; granulocyte macrophage colony-stimulating factor; H6pd, hexose-6-phosphate dehydrogenase; Hk2, hexokinase 2; IL, interleukinIL-6R; interleukin-6 receptor; Il18rap, interleukin 18 receptor accessory protein; IP-10, interferon gamma-induced protein 10; JAK, Janus kinase; KIR, killer immunoglobulin-like receptor; Klra1, killer lectin-like receptor subfamil...

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“…Adipocytes, as well as the macrophages embedded in fat tissue, are known to be a major source of the IL-6 found in blood, especially in the non-inflammatory, healthy state (Coppack, 2007; Fried et al, 1998; Khaodhiar et al, 2004; Suganami and Ogawa, 2010; Weisberg et al, 2003; Wisse, 2004). The adipokine leptin also stimulates the release of IL-6 from leukocytes and macrophages (Agrawal et al, 2011; Behrendt et al, 2010; Kredel et al, 2013). Although these biological pathways often interact in a bidirectional and reciprocal manner, there is considerable evidence to suggest that adiposity exerts a far greater influence on inflammatory physiology (Miller, 2003; Welsh et al, 2010).…”

Section: Introductionmentioning

confidence: 99%