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PMN treated with control-CM or H37Rv-CM and then exposed to i-H37Rv showed a higher CD11b expression than N-T PMN, while M-CM did not alter iH37Rv-induced CD11b upregulation (Figure 3(b)).
In contrast, M-CM was not able to enhance ROS production in response to PMA or i-H37Rv.
Pretreatment of PMN with control-CM and M-CM diminished the percentage of late apoptotic PMN when compared to nontreated cells while H37Rv-CM did not.
While PMN exposed to M-CM displayed similar IL-8 amounts when compared to N-T PMN, preincubation with control-CM or H37Rv-CM showed lower IL-8 secretion upon H37Rv infection.
Instead, the activation of PMN upon i-H37Rv stimulation was altered and it was dependent on the sources of CM, while H37Rv-CM increased CD11b expression, M-CM did not, and it was dependent on the content of TNF-[alpha] of each CM.
However, we observed that while control-CM and H37Rv-CM did not modify bacterial growth, M-CM enhanced H37Rv intracellular growth in PMN.
Interestingly, PMN preincubated with M-CM secreted higher IL-8 than that with the noninfected ones, which could be influencing the PMN recruitment.
Conditioned media (CM) from 18 h cultured uninfected (control-CM) or H37Rv- or M-infected Calu-6 cells (H37Rv-CM and M-CM) were tested for (a) TGF-[beta], TNF-[alpha], GM-CSF, and IL-8 by ELISA.
Freshly, PMN (n = 7) were incubated for 1.5 h with (a) RPMI 1640 plus (N-T) or with conditioned media (CM) from Calu-6 cells infected with H37Rv or M (H37Rv-CM and M-CM) or noninfected (control-CM) or (b) additionally with H37Rv-CM-depleted TNF-[alpha] (depl-H37Rv-CM), M-CM plus TNF-[alpha] (M-CM-TNF-[alpha]), or TNF-[alpha] (20ng/ml).
PMN (n = 6) cultured for 1.5 h alone (N-T) or with control-CM, H37Rv-CM, or M-CM in the presence or not of cytochalasin B were incubated for 1 h with FITC- labeled i-H37Rv.
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