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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Acute Penicillium marneffei infection stimulates host M1/M2a macrophages polarization in BALB/C mice
Xiaoying Dai1, Congzheng Mao1, Xiuwan Lan2
1Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China.
Background:
Penicillium marneffei (P. marneffei) is a thermally dimorphic fungus pathogen that causes fatal infection. Alveolar macrophages are innate immune cells that have critical roles in protection against pulmonary fungal pathogens and the macrophage polarization state has the potential to be a deciding factor in disease progression or resolution. The aim of this study was to investigate mouse alveolar macrophage polarization states during P. marneffei infection.
Results:
We used enzyme-linked immunosorbent (ELISA) assays, quantitative real-time PCR (qRT-PCR), and Griess, arginase activity to evaluate the phenotypic markers of alveolar macrophages from BALB/C mice infected with P. marneffei. We then treated alveolar macrophages from infected mice with P. marneffei cytoplasmic yeast antigen (CYA) and investigated alveolar macrophage phenotypic markers in order to identify macrophage polarization in response to P. marneffei antigens. Our results showed: i) P. marneffei infection significantly enhanced the expression of classically activated macrophage (M1)-phenotypic markers (inducible nitric oxide synthase [iNOS] mRNA, nitric oxide [NO], interleukin-12 [IL-12], tumor necrosis factor-alpha [TNF-α]) and alternatively activated macrophage (M2a)-phenotypic markers (arginase1 [Arg1] mRNA, urea) during the second week post-infection. This significantly decreased during the fourth week post-infection. ii) During P. marneffei infection, CYA stimulation also significantly enhanced the expression of M1 and M2a-phenotypic markers, consistent with the results for P. marneffei infection and CYA stimulation preferentially induced M1 subtype.
Conclusions:
The data from the current study demonstrated that alveolar macrophage M1/M2a subtypes were present in host defense against acute P. marneffei infection and that CYA could mimic P. marneffei to induce a host immune response with enhanced M1 subtype. This could be useful for investigating the enhancement of host anti-P. marneffei immune responses and to provide novel ideas for prevention of P. marneffei-infection.
Insights
Penicillium marneffei infection impacts alveolar macrophage polarization, promoting both M1 and M2a subtypes. Cytoplasmic yeast antigen (CYA) also induces these subtypes, preferentially M1, aiding host defense against this fungal pathogen.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Penicillium marneffei (P. marneffei) is a thermally dimorphic fungus causing fatal infections.
- Alveolar macrophages are crucial innate immune cells in pulmonary defense.
- Macrophage polarization state influences P. marneffei infection outcomes.
Purpose of the Study:
- To investigate mouse alveolar macrophage polarization during P. marneffei infection.
- To determine the effect of P. marneffei cytoplasmic yeast antigen (CYA) on macrophage polarization.
Main Methods:
- Enzyme-linked immunosorbent assays (ELISA), qRT-PCR, Griess, and arginase activity assays were used.
- Alveolar macrophages from BALB/C mice infected with P. marneffei were analyzed.
- Macrophages were stimulated with P. marneffei CYA to assess polarization markers.
Main Results:
- P. marneffei infection enhanced M1 (iNOS, NO, IL-12, TNF-α) and M2a (Arg1, urea) markers in the second week, decreasing by the fourth.
- CYA stimulation also enhanced M1 and M2a markers, mirroring infection effects.
- CYA preferentially induced the M1 macrophage subtype.
Conclusions:
- Alveolar macrophage M1/M2a subtypes are involved in host defense against acute P. marneffei infection.
- P. marneffei CYA mimics the fungus in inducing host immune responses, particularly M1 polarization.
- Findings offer insights for enhancing anti-P. marneffei immunity and prevention strategies.
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