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Macrophages are innate immunity cells essential for systems homeostasis. They can be modulated by stimuli present in the microenvironment and by other cells, such as B-1 cells, and can alter effector and phenotypic actions. B-1 cells spontaneously secrete IgM and IL-10 that can functionally modulate macrophages. Cytokines present in the microenvironment induce the polarization of macrophages to different phenotypes during the activation. Macrophages can recognize microorganisms through PRR, triggering activation that lead to reactive oxygen species (ROS) and nitric oxide (NO) production. In addition to their microbicidal activity, macrophages play a pivotal role in the initiation of adaptive immunity, since these cells present antigen to T lymphocytes. In this work, the functional and phenotypic differences between peritoneal macrophages from BALB/c and XID mice-deficient in B-1 cells, were evaluated. Peripheral blood leukometry showed that there was no difference in the percentage of monocytes in peripheral blood. However, cytometry of the peritoneal cavity showed a reduction in the percentage of macrophages in XID mice, accompanied by an increase in the expression of major histocompatibility complex II. Functional analysis, using a phagocytosis assay, demonstrated that macrophages from XID and BALB/c mice have no difference on phagocytosis ability, however macrophages from XID mice have a lower number of phagocytosed yeasts. Using the Griess method and a probe as a general indicator of oxidative stress, we quantified NO and ROS, respectively, as molecules involved in microbicidal activity. Our results showed that macrophages from XID mice spontaneously produce high levels of NO compared to macrophages from BALB/c mice. ROS evaluation showed that in the presence of stimulation, XID macrophages produce more ROS than BALB/c macrophages. Taken together, these data suggest that macrophages from XID mice display a pro-inflammatory profile.
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