Fig 1: Role of autophagy in BHB induced depression of co-localization between CD11b and LC3. Rapamycin (100 nM, 2 h) was used to activate autophagy. (A) Immunofluorescence data showed the co-localization of CD11b with LC3 in neutrophils. Magnification 400×. Scale bar = 10 μm. Nuclei/DAPI in blue, CD11b in green, and LC3 in red. Images here represent the typical common phenotype of each group. (B) Pearson’s correlation coefficient (r) between CD11b and LC3. Data were expressed as the mean ± SEM. A two-way analysis of variance (ANOVA) was performed to analyze differences between BHB and RARA, including a Bonferroni post-hoc analysis. Two-way ANOVA showed a significant difference in BHB × RAPA interaction (P < 0.01), including a Bonferroni post-hoc analysis. **P < 0.01 as statistically highly significant. CON, control; BHB, β-hydroxybutyrate; RAPA, rapamycin; LC3, microtubule associated proteins 1A/1B light chain 3; CD11b, integrin alpha-M precursor; SEM, standard error of the mean.
Fig 2: Point graph of the number of CD11b+MHC II+ DCs in the nasal mucosa, nasopharyngeal tonsil and soft palate tonsil following intranasal administration of B. subtilis. The data are presented as the mean ± standard error of the mean (n=4/group). The error bars indicate the standard error. *P<0.05. CD, cluster of differentiation; MHC, major histocompatibility complex; DC, dendritic cells.
Fig 3: Effect of BHB with different stimulated times on the adhesion of bovine neutrophils. Neutrophils were treated with 1.6 mM BHB for 0, 1, 2, 4, and 6 h, respectively. (A) Quantitation of the number of adherent neutrophils. (B-I) Protein abundance of membrane and total CD11a, CD11b, and CD18. Representative blots in both groups were shown in B-C. The quantification was shown in D-I. (J) Neutrophils were treated with 1.6 mM BHB for 2h. mRNA abundance of ITGAL, ITGAM, and ITGB2. For WB experiments, β-actin was used to normalize the total protein abundance, while Na+/K+ ATPase was used to normalize membrane protein abundance; for qRT-PCR experiments, β-Actin and YWHAZ were used to normalize mRNA abundance. Data were expressed as the mean ± SEM. Data were analyzed with a one-way ANOVA with subsequent Bonferroni correction or independent-samples t-tests. **P < 0.01 as statistically highly significant. BHB, β-hydroxybutyrate; CD11b, integrin alpha-M precursor; CD11a, integrin alpha-L precursor; CD18, integrin beta-2 precursor; ITGAL, integrin subunit alpha L; ITGAM, integrin subunit alpha M; ITGB2, integrin subunit beta 2; YWHAZ, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta; SEM, standard error of the mean.
Fig 4: Mucosal CD11b+ cellular expression in GI biopsies of cats with IBD compared to cats with small cell GI LSA in the ileum and colon (total = 28 cats; IBD = 14 cats; small cell GI LSA = 14 cats). Boxes show lowest, median, and upper quartiles. Whiskers represent 1.5 of the interquartile range, with means denoted by the black rhombi and outliers denoted by the black circles. Median mucosal CD11b+ myeloid cell counts are significantly higher in the ileal (median = 503; P = .012) and colonic (median = 77; P < .0001) biopsies of cats with small cell GI LSA compared to the ileal (median = 82.5) and colonic (median = 15) biopsies of cats with IBD
Fig 5: Representative images of Cd11b staining in dentate gyrus left and cornu amonis 1 (Right) regions of the hippocampus in male C57BL/6J (A) and DAT-Cnr2 cKO (B) male mice. Cd11b immunofluorescence (green).
Supplier Page from Abcam for Anti-CD11b antibody