Association among inflammaging, body composition, physical activity, and physical function tests in physically active women

BackgroundInflammaging is a phenomenon that has been associated with the development and progression of sarcopenia and frailty syndrome. According to the literature, on the one side, the increase in body fat is associated with a systemic pro-inflammatory status, which consequently favors inflammaging, and on the other side, the regular practice of physical exercise can mitigate the development of this scenario. Therefore, here, we aimed to evaluate the association between inflammaging and physical factors, both body and functional, in a group of physically active older women.MethodsSeventy older women (mean age 72.66 ± 6.17 years) participated in this observational cross-sectional and were separated into the eutrophic, overweight, and obese groups. It was assessed: by bioimpedance—body fat percentage (Fat%) and total (Fat kg), skeletal muscle mass (muscle), and free fat mass both in percentage (FFM%) and total (FFMkg); by the International Physical Activity Questionnaire (IPAQ)—the time of moderate-intensity physical activity per week; by physical tests—handgrip (HG), sit-up-stand-on-the-chair in 5 repetitions (Sit-up) and vertical squat jump test (SJ); in addition to the determination of serum cytokine concentration (IL-6, TNF-α, IL-10, and IL-8), and also body mass index (BMI) and calf circumference (Calf).ResultsHigher FFM% and lower body fat (both kg and %) were found in the eutrophic group than in the other groups. The eutrophic group also performed more weekly physical activity, jumped higher, and presented not only higher serum IL-6 concentration but also an increased ratio of IL-10/IL-6, IL-10/TNF-α, IL-10/IL-8 as compared to the values found in the overweight group. The obese group presented higher body fat (kg and %) and lower FFM% than the other groups and also higher serum IL-6 concentration than the overweight group. Interestingly, several significant negative and positive correlations between body composition, physical tests, and serum cytokine concentrations were found in the eutrophic and obese groups.ConclusionWhile the eutrophic older women group showed a remarkable regulation of the systemic inflammatory status with positive associations in the physical parameters assessed, the overweight and obese groups presented impairment regulations of the inflammaging, which could be related to less weekly physical activity and higher body fat

Diabetes mellitus increases the susceptibility to encephalitozoonosis in mice.

Microsporidiosis are diseases caused by opportunistic intracellular fungi in immunosuppressed individuals, as well as in transplanted patients, the elderly and children, among others. Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia and decreased T cell response, neutrophil function, humoral immunity failure, increasing the susceptibility to infections. Here, we investigated the susceptibility of streptozotocin (STZ)-induced type I diabetic and/or immunosuppressed mice to encephalitozoonosis by Encephalitozoon cuniculi. Microscopically, granulomatous hepatitis, interstitial pneumonia and pielonephritis were observed in all infected groups. STZ treatment induced an immunossupressor effect in the populations of B (B-1 and B2) and CD4+ T lymphocytes. Moreover, infection decreased CD4+ and CD8+ T lymphocytes and macrophages of DM mice. Furthermore, infection induced a significant increase of IL-6 and TNF-α cytokine serum levels in DM mice. IFN-γ, the most important cytokine for the resolution of encephalitozoonosis, increased only in infected mice. In addition to the decreased immune response, DM mice were more susceptible to encephalitozoonosis, associated with increased fungal burden, and symptoms. Additionally, cyclophosphamide immunosuppression in DM mice further increased the susceptibility to encephalitozoonosis. Thus, microsporidiosis should be considered in the differential diagnosis of comorbidities in diabetics

Spleen immune cell analysis.

<p>Evaluation of B-2 (CD23⁺CD19⁺) cells, CD4⁺ (CD19^-CD8^-CD4+), and CD8⁺ (CD19^-CD4^-CD8⁺) T lymphocytes and macrophages (CD19^-F4/80⁺CD11b⁺) in spleen Cy immunosuppressed and STZ-induced DM mice infected with <i>E</i>. <i>cuniculi</i> compared with its controls. Two ways variance analysis (ANOVA) revealed * p<0,05.</p

Peritoneal immune cell analysis.

<p>Evaluation of B-1 (CD23^-CD19⁺), B-2 (CD23⁺CD19⁺), Pre-B-1CDP (CD19⁺CD11b⁺F4/80⁺) cells, CD4⁺ (CD19^-CD8^-CD4+), CD8⁺ (CD19^-CD4^-CD8⁺) T lymphocytes and macrophages (CD19^-F4/80⁺CD11b⁺) from PerC of STZ-induced DM mice infected with <i>E</i>. <i>cuniculi</i> compared with its controls. Two ways variance analysis (ANOVA) revealed * p<0,05.</p

Morphometric analyses of hepatic lesions from <i>E</i>. <i>cuniculi</i> infected mice.

<p>Lesions´ area of the liver from animals treated or not with cyclophosphamide (Cy) and treated or not with STZ to development of Type 1 Diabetes mellitus (DM).</p

Photomicrographs of histopathological lesions in <i>E</i>. <i>cuniculi Infected</i> and <i>DM-Infected</i> mice.

<p>Liver—mononuclear inflammatory infiltrate located at A) parenchyma, B) portal vein, C) under capsule and D) <i>E</i>. <i>cuniculi</i> clusters into inflammatory infiltrate. Lungs–E and F) interstitial pneumonia. Kidney–G) pyelonephritis and H) nephritis (HE).</p

IL-6, IFN-γ and TNF-α cytokines levels in the serum of STZ-induced DM mice infected with <i>E</i>. <i>cuniculi</i> compared with its controls mice.

<p>+ and–means presence and absence, respectively, of STZ treatment and <i>E</i>. <i>cuniculi</i> infection. Two ways variance analysis (ANOVA) revealed * p<0,05 and **** p<0,0001.</p

Blood glucose, body weight and fungal burden parameters in mice immunosuppressed with cyclophosphamide (Cy): <i>Cy-Infected</i>, <i>Cy-Uninfected</i>, <i>DM-Cy-Uninfected</i> and <i>DM-Cy-Infected</i>.

<p>A) Blood glucose variation between immunosuppressed groups during all experimental period. B) Body weight variation of <i>DM-Cy-Infected</i> and Cy-<i>Infected</i> mice and its respective controls. C) Fungal burden in the PerC of <i>E</i>. <i>cuniculi</i> infected mice. + and–means presence or absence, respectively, of Cy treatment and <i>E</i>. <i>cuniculi</i> infection x means time folds compared to <i>Uninfected</i> (-/-) group. Non parametric <i>t-test</i> showed * p<0,05 and ** p<0,01 (A e B) and One way variance analysis (ANOVA) revealed $ p<0,05 comparing with uninfected groups and ** p<0,01 compared to the other groups.</p

Blood glucose, body weight and fungal burden parameters in mice of experimental groups: <i>Infected</i>, <i>Uninfected</i>, <i>DM-Uninfected</i> and <i>DM-Infected</i>.

<p>A) Blood glucose variation between groups during all experimental period. B) Body weight variation of <i>DM-Infected</i> and <i>Infected</i> mice and its respective controls. One way variance analysis (ANOVA) with Tukey post test showed *** p < 0,01. C) Fungal burden in <i>Infected</i> and <i>DM-Infected</i> mice by <i>E</i>. <i>cuniculi</i>. Non-parametric <i>t-test</i> showing * p<0.01, comparing each group of each period, separately. D) <i>E</i>. <i>cuniculi</i> spores observed in the PerC of <i>DM-Infected</i> mice stained by Calcofluor fluorescent staining.</p