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Therapeutic Efficacy of an Anti-P116-661 Polyclonal Antibody Against Mycoplasma pneumoniae Infection
Yiting Zhang1, Xinqi Geng1, Yan Liu1
1Anhui Provincial Key Laboratory of Zoonoses, Department of Microbiology and Parasitology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China.
The aim of this study was to investigate the therapeutic potential of a polyclonal antibody against the Mycoplasma pneumoniae (MP) P116-661 protein. A polyclonal antibody against the P116-661 protein was obtained by immunizing New Zealand white rabbits, and its therapeutic effects were systematically evaluated by various experimental methods. An immunofluorescence assay was used to detect the inhibitory effect of the P116-661 polyclonal antibody on the adhesion of MP cells to A549 cells. ELISAs and Western blotting were used to analyze the expression levels of inflammatory factors, such as IL-6 and TNF-α, in Beas-2b cells and model mice after MP infection. HE staining was used to observe pathological changes in the lung tissue of the infected mice. The results showed that the P116-661 polyclonal antibody effectively inhibited the adhesion of MP cells to A549 cells. It significantly reduced the secretion levels of inflammatory factors, such as IL-6 and TNF-α, in Beas-2b cells and mice after MP infection. Moreover, the antibody significantly improved the pathological damage to the lungs that was caused by MP infection in mice. This study confirms that the P116-661 polyclonal antibody has good therapeutic effects in vitro and in vivo, providing a new experimental basis for immunotherapy against MP infection.
The aim of this study was to investigate the therapeutic potential of a polyclonal antibody against the Mycoplasma pneumoniae (MP) P116-661 protein. A polyclonal antibody against the P116-661 protein was obtained by immunizing New Zealand white rabbits, and its therapeutic effects were systematically evaluated by various experimental methods. An immunofluorescence assay was used to detect the inhibitory effect of the P116-661 polyclonal antibody on the adhesion of MP cells to A549 cells. ELISAs and Western blotting were used to analyze the expression levels of inflammatory factors, such as IL-6 and TNF-α, in Beas-2b cells and model mice after MP infection. HE staining was used to observe pathological changes in the lung tissue of the infected mice. The results showed that the P116-661 polyclonal antibody effectively inhibited the adhesion of MP cells to A549 cells. It significantly reduced the secretion levels of inflammatory factors, such as IL-6 and TNF-α, in Beas-2b cells and mice after MP infection. Moreover, the antibody significantly improved the pathological damage to the lungs that was caused by MP infection in mice. This study confirms that the P116-661 polyclonal antibody has good therapeutic effects in vitro and in vivo, providing a new experimental basis for immunotherapy against MP infection.
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