Lei Han

Dr. Lei Han

orcid

Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2021 in Microbial Pathogenesis
Verified
Journal Article
Open access
MAMona Mohamed Al-Shamiri
Mona Mohamed Al-Shamiri
SZSirui Zhang
Sirui Zhang
PMPeng Mi
Peng Mi
YLYuqing Liu
Yuqing Liu
MXMeng Xun
Meng Xun
YCYanjiong Chen
Yanjiong Chen
Acinetobacter baumannii is an important pathogen in clinical. The factors of biofilm formation, antibiotic resistance and motility contribute great to A. baumannii in persisting in stressed environment, and further leads to nosocomial infections. 70 A. baumannii clinical isolates were investigated for their clinical characteristics of infection. Among the tested strains, 54 (77.1%) isolates were obtained from ICUs, with the frequency of multidrug-resistance (MDR) at 55.7%, and that of extensively drug-resistance (XDR) at 31.4%. 97.1% of the clinical isolates could form biofilms, in which 4.3% possessed weak biofilm formation ability, while 41.4% and 51.4% were moderate and strong biofilm producers, respectively. A strong correlation between antibiotic resistance and biofilm formation ability was found that all the resistant strains could form biofilms, with the majority in moderate and strong levels, but 2.9% sensitive isolates had no such ability. However, the sensitive strains that could produce biofilms showed stronger biofilm formation capacity in the early stage before 24 h compared to the resistant isolates, though they became weaker afterwards. 24 biofilm-related genes and two blaOXA genes were found in both biofilm-forming and non-biofilm-forming strains, but with higher prevalence in the strains that could produce biofilms. No correlation was detected between twitching motility with antibiotic susceptibility or biofilm formation. These results raised a viewpoint that examining timepoint is a key factor for determining the biofilm formation ability, and further highlighted the importance of the appropriate surveillance and control measures in preventing the emergence and transmission of MDR and XDR A. baumannii.

13 April 2023 in Microbiology Spectrum
Verified
Journal Article
Open access
MAMona Mohamed Al-Shamiri
Mona Mohamed Al-Shamiri
JWJingdan Wang
Jingdan Wang
SZSirui Zhang
Sirui Zhang
PLPu Li
Pu Li
WOWoodvine Otieno Odhiambo
Woodvine Otieno Odhiambo
SHShaoshan Han
Shaoshan Han
A. baumannii biofilm is a significant virulence factor that causes the biofilm colonization of invasive illnesses. Rising bacterial resistance to synthetic antimicrobials has prompted researchers to look at natural alternatives, such as probiotics and their derivatives.

17 January 2023 in Antibiotics
Verified
Journal Article
Open access
PDF file
PLPu Li
Pu Li
SZSirui Zhang
Sirui Zhang
JWJingdan Wang
Jingdan Wang
MAMona Mohamed Al-Shamiri
Mona Mohamed Al-Shamiri
BHBei Han
Bei Han
LHLei Han
Lei Han
Infections led by Acinetobacter baumannii strains are of great concern in healthcare environments due to the strong ability of the bacteria to spread through different apparatuses and develop drug resistance. Severe diseases can be caused by A. baumannii in critically ill patients, but its biological process and mechanism are not well understood. Secretion systems have recently been demonstrated to be involved in the pathogenic process, and five types of secretion systems out of the currently known six from Gram-negative bacteria have been found in A. baumannii. They can promote the fitness and pathogenesis of the bacteria by releasing a variety of effectors. Additionally, antibiotic resistance is found to be related to some types of secretion systems. In this review, we describe the genetic and structural compositions of the five secretion systems that exist in Acinetobacter. In addition, the function and molecular mechanism of each secretion system are summarized to explain how they enable these critical pathogens to overcome eukaryotic hosts and prokaryotic competitors to cause diseases.

27 April 2022 in Microbiology Spectrum
Verified
Journal Article
Open access
LHLei Han
Lei Han
YGYiyuan Gao
Yiyuan Gao
YLYuqing Liu
Yuqing Liu
SYSiyu Yao
Siyu Yao
SZShuyan Zhong
Shuyan Zhong
SHShaoshan Han
Shaoshan Han
Acinetobacter baumannii can develop various resistance mechanisms to carbapenems. However, the factors involved in the evolutionary process that leads from transition to the sensitive to resistant phenotype are not clear.

Verified
Journal Article
Open access
PDF file
JWJun Wang
Jun Wang
XMXinxin Ma
Xinxin Ma
JLJing Li
Jing Li
LSLu Shi
Lu Shi
LLLijuan Liu
Lijuan Liu
BHBei Han
Bei Han
Methicillin-resistant Staphylococcus aureus (MRSA) is responsible for skin and soft tissue infections with multi-resistance to many antibiotics. It is thus imperative to explore alternative antimicrobial treatments to ensure future treatment options. Nisin (NIS), an antibacterial peptide produced by Lactococcus lactis, was selected to combine with Oxacillin (OX), to evaluate the antimicrobial effect and potential mechanism against MRSA. The synergistic antimicrobial effect of OX and NIS was verified by Minimal Inhibitory Concentration (MIC) assays, checkerboard analysis, time-kill curve, biofilm producing ability, and mice skin infection model in vivo. For the potential synergistic antimicrobial mechanism, the microstructure and integrity change of MRSA cells were determined by Scanning and Transmission Electron Microscope (SEM and TEM), intracellular alkaline phosphatase activity and propidium iodide staining were assayed; And transcription of mecA, main gene of MRSA resistant to OX, were detected by qRT-PCR. The results showed NIS could restore the sensitivity of MRSA to OX and inhibit biofilm production; OX + NIS can make MRSA cell deform; NIS may recover OX sensitivity by inhibiting the transcription of mecA. In vivo, mice skin infection models indicate that OX + NIS can substantially alleviate MRSA infections. As a safe commercially available biological compound, NIS and the combination of antibiotics are worth developing as new anti-MRSA biomaterials.

7 February 2024 in Frontiers in Cellular and Infection Microbiology
Verified
Journal Article
Open access
PLPu Li
Pu Li
SZSirui Zhang
Sirui Zhang
JWJingdan Wang
Jingdan Wang
MAMona Mohamed Al-Shamiri
Mona Mohamed Al-Shamiri
KLKai Luo
Kai Luo
LHLei Han
Lei Han
Introduction: The type VI secretion system (T6SS) is a crucial virulence factor in the nosocomial pathogen Acinetobacter baumannii. However, its association with drug resistance is less well known. Notably, the roles that different T6SS components play in the process of antimicrobial resistance, as well as in virulence, have not been systematically revealed.Methods: The importance of three representative T6SS core genes involved in the drug resistance and virulence of A. baumannii, namely, tssB, tssD (hcp), and tssM was elucidated.Results: A higher ratio of the three core genes was detected in drug-resistant strains than in susceptible strains among our 114 A. baumannii clinical isolates. Upon deletion of tssB in AB795639, increased antimicrobial resistance to cefuroxime and ceftriaxone was observed, alongside reduced resistance to gentamicin. The ΔtssD mutant showed decreased resistance to ciprofloxacin, norfloxacin, ofloxacin, tetracycline, and doxycycline, but increased resistance to tobramycin and streptomycin. The tssM-lacking mutant showed an increased sensitivity to ofloxacin, polymyxin B, and furazolidone. In addition, a significant reduction in biofilm formation was observed only with the ΔtssM mutant. Moreover, the ΔtssM strain, followed by the ΔtssD mutant, showed decreased survival in human serum, with attenuated competition with Escherichia coli and impaired lethality in Galleria mellonella.Discussion: The above results suggest that T6SS plays an important role, participating in the antibiotic resistance of A. baumannii, especially in terms of intrinsic resistance. Meanwhile, tssM and tssD contribute to bacterial virulence to a greater degree, with tssM being associated with greater importance.