Clinical Isolates of Mycobacterium tuberculosis Differ in Their Ability to Induce Respiratory Burst and Apoptosis in Neutrophils as a Possible Mechanism of Immune Escape

Figure 4

Role of MAP kinases and reactive oxygen species in PMN apoptosis induced by Mtb strains. (a) PMN (3 × 10⁶/mL) were cultured in media alone (control, —) or stimulated with Mtb strains at 1 : 2 Mtb : PMN ratio for 18 h, in the presence or absence of specific inhibitors for p38 and ERK (SB203580 and PD98059, resp.), and an oxidase inhibitor DPI. Thereafter, Annexin V-FITC (AV-FITC) binding was measured by flow cytometry. Results are expressed as media ± SEM (𝑛=12). Statistical differences: Control versus LAM: ^∗∗∗𝑃<0.001, control versus H: ^∗∗𝑃<0.01, control versus H37Rv: ^∗𝑃<0.05; H37Rv, LAM and H versus SB: ^#𝑃<0.01; H37RV, LAM and H versus DPI: ^𝜎𝑃<0.001; M versus PD: ^𝜑𝑃<0.01. (b) PMN were treated with 10 mM H₂O₂ 15 min before Mtb challenge and thereafter PMN were cultured as described in (a). After 18 h-culture, Annexin V-FITC (AV-FITC) positive PMN was measured by flow cytometry. A representative experiment out of four is displayed.

(a)

(b)