Background: Macrophages are heterogenous phagocytic cells with an important role in the innate immunity. They are, also, significant contributors in the adaptive immune system. Macrophages are the most abundant immune cells in the lung during allergic asthma, which is the most common chronic respiratory disease of both adults and children. Macrophages activated by Th1 cells are known as M1 macrophages while those activated by IL-4 and IL-13 are called alternatively activated macrophages (AAM) or M2 cells. AAM are subdivided into four distinct subtypes (M2a, M2b, M2c and M2d), depending on the nature of inducing agent and the expressed markers. Body: IL-4 is the major effector cytokine in both alternative activation of macrophages and pathogenesis of asthma. Thus, the role of M2a macrophages in asthma is a major concern. However, this is controversial. Therefore, further studies are required to improve our knowledge about the role of IL-4-induced macrophages in allergic asthma, through precisive elucidation of the roles of specific M2a proteins in the pathogenesis of asthma. In the current review, we try to illustrate the different functions of M2a macrophages (protective and pathogenic roles) in the pathogenesis of asthma, including explanation of how different M2a proteins and markers act during the pathogenesis of allergic asthma. These include surface markers, enzymes, secreted proteins, chemokines, cytokines, signal transduction proteins and transcription factors. Conclusions: AAM is considered a double-edged sword in allergic asthma. Finally, we recommend further studies that focus on increased selective expression or suppression of protective and pathogenic M2a markers.

Both Gram-Positive and Gram-Negative bacteria can secrete outer membrane vesicles (OMVs) in their growth and metabolism process. Originally, OMVs were considered as a by-product of bacterial merisis. However, many scientists have reported the important role of OMVs in many fields recently. In this review, we briefly introduce OMVs biological functions and then summarize the findings about the OMVs interactions with host cells. At last, we will make an expectation about the prospects of the application of OMVs as vaccines.

BackgroundType 2 innate lymphoid cells (ILC2s), characterized by secreting type 2 cytokines, regulate multiple immune responses. ILC2s are found in different tumor tissues and ILC2-derived interleukin (IL)-4, IL-5, and IL-13 act on the cells in tumor microenvironment to participate in tumor progression. ILC2s are abundant in colorectal cancer (CRC) tissue, but the role of ILC2s in CRC remains unclear. MethodsILC2s were sorted from the spleen using microbeads combined with flow cytometry and tumor infiltrating CD8 + T cells were isolated from tumor tissue by microbeads. Flow cytometry and immunofluorescence were used to detect the percentage of ILC2s and CD8 + T cells in the spleen and CRC tissue. Effects of IL-9 and IL-9-stimulated CD8 + T cells on CT26 cells were measured by proliferation, apoptosis, and migration assays in vitro. GEPIA was used to detect the ILC2s chemokines in CRC tissue and adjacent normal tissue. ResultsWe found that ILC2s were increased in CRC tissue compared with the adjacent normal tissue. In vitro experiments showed that IL-9 could activate CD8 + T cells to promote the death of CT26 cells. ILC2s were the main IL-9-secreting cells in CRC tissue as shown by flow cytometry analysis. In vivo experiments showed that neutralizing ILC2s promoted the tumor growth, while tumor inhibition occurred by intravenous injection of IL-9. ConclusionsOur results demonstrated that ILC2-derived IL-9 activated CD8 + T cells to promote anti-tumor effects in CRC.Th9 cells inhibit the development of melanoma and breast cancer by secreting 33]. In addition, Th9-derived IL-9 promotes the expansion of CD8 + T cells through IL-9 receptor (IL-9R) in CRC [34]. However, the main IL-9-producing cell subset in CRC remains unclear.Here we investigated the role of ILC2s and IL-9 in the CRC progression. The IL-9-producing cell subset in CRC tissue was also detected. We hypothesized that ILC2-derived IL-9 could exert an antitumor role in CRC. Materials And Methods Cell line and cell cultureThe murine CRC cell line CT26 was purchased from the American Type Culture Collection (Manassas, VA, USA). Cells were cultured in a humidified incubator with 5% CO2 at 37 °C. AnimalsFemale BALB/c mice (6-8 weeks, 18-22 g) were purchased from the Animal Center of Yangzhou University (Yangzhou, China) and the Animal Center of Jiangsu University (Zhenjiang, China). Mice were housed in cages and bred in pathogen-free rooms with a temperature of 23 °C ± 2 °C and relative humidity of 55%±10%. All animal experiments complied with the protocol of Jiangsu University Animal Ethics and Experimentation Committee.

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Acinetobacter baumannii, as a nonfermentation Gram-negative bacterium, mainly cause nosocomial infections in critically ill patients. With the widespread of multidrug-resistant Acinetobacter baumannii, the urgency of developing effective therapy options has been emphasized nowadays. Outer membrane vesicles derived from bacteria show potential vaccine effects against bacterial infection in recent study. Our present research is aimed at investigating the mechanisms involved in immune protection of mice after outer membrane vesicle immunization. As our data showed, the outer membrane vesicle from an Acinetobacter baumannii clinical strain could activate bone marrow-derived dendritic cells (BMDCs) to promote Th2 activity together with humoral immune responses to Acinetobacter baumannii-induced sepsis, which might enlighten people to have a better understanding of OMVs' role as a vaccine to prevent bacterial infections.

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Type 9 T-helper (Th9) cells are associated with atopic and inflammatory diseases. Their increased levels and functions contribute to a number of inflammatory disorders, where they are accompanied by enhanced Th2-cell activity. However, there is currently no consensus regarding the association between Th9 and Th2 cells. Th9 cells may be induced from naïve T (Th0) cells under specific polarization conditions in vitro, a process driven by the addition of specific cytokines. In the present study, Th0 cells were cultured under Th9-polarizing conditions to promote differentiation into interleukin (IL)-4 + IL-9or IL-4 -IL-9 + T cells after 3 or 5 days in culture, respectively; the mRNA expression levels of IL-9 and IL-4 were consistent with the induced cell types. Simultaneously, the levels of interferon-regulatory factor 4 (IRF-4) and Smad3/Smad4 were significantly increased following Th9-cell polarization. It was therefore proposed that Th2 cells may be generated in the early stages of Th9-cell differentiation, and then ultimately differentiate into Th9 cells via the Smad3/Smad4 and IRF-4 activation pathway.

The accumulation of airway apoptotic cells may be an important factor causing airway hyper-responsiveness (AHR). Whether the apoptotic cells can be promptly removed is related to the occurrence and course of asthma. In recent years, studies have shown that Rac1 is involved in many cellular biological activities including the formation and elimination of apoptotic cells. In this study, based on the analysis of airway local cells and related factors in asthmatic mice, we evaluated the expression of Rac1 in airway epithelial cells or phagocytes and analysed its relationship with the incidence of apoptosis or scavenging of apoptotic cells. Our data showed that the expression level of Rac1 in asthmatic mice decreased significantly, while the expression of IL-33 increased obviously. The airway epithelial cell line was stimulated by curcumin at 50 μmol/L for 24-48 hours; more than 50% of the cells were apoptotic, and of which, about 20% were late apoptosis. Rac1 inhibitor (NSC23766) can enhance the apoptosis effect. In addition, the ability of phagocytosis and migration in the epithelial cells or macrophages was increased following the application of Rac1 inhibitors or specific siRNA in a dose-dependent manner, and the expression level of IL-33 was simultaneously increased after blocking Rac1. It is suggested that the down regulation of Rac1 in asthma may contribute to the apoptosis of airway epithelial cells and affect the clearance of apoptotic cells, which will lead to the aggregation of the apoptotic cells in the respiratory tract and participate in AHR.