The crosstalk between intestinal bacterial microbiota and immune cells in colorectal cancer progression

Different types of cells that are involved in tumor immunity play a significant part in antitumor therapy. The intestinal microbiota consist of the trillions of diverse microorganisms that inhabit the gastrointestinal tract. Recently, much emphasis has been paid to the link between these symbionts and colorectal cancer (CRC). This association might be anything from oncogenesis and cancer development to resistance or susceptibility to chemotherapeutic medicines. Cancer patients have a significantly different microbial composition in their guts compared to healthy persons. The microbiome may play a role in the development and development of cancer through the modulation of tumor immunosurveillance, as shown by these studies; however, the specific processes underlying this role are still poorly understood. This review focuses on the relationship between the intestinal bacterial microbiota and immune cells to determine how the commensal microbiome influences the initiation and development of CRC (AU)

The crosstalk between intestinal bacterial microbiota and immune cells in colorectal cancer progression.

Different types of cells that are involved in tumor immunity play a significant part in antitumor therapy. The intestinal microbiota consist of the trillions of diverse microorganisms that inhabit the gastrointestinal tract. Recently, much emphasis has been paid to the link between these symbionts and colorectal cancer (CRC). This association might be anything from oncogenesis and cancer development to resistance or susceptibility to chemotherapeutic medicines. Cancer patients have a significantly different microbial composition in their guts compared to healthy persons. The microbiome may play a role in the development and development of cancer through the modulation of tumor immunosurveillance, as shown by these studies; however, the specific processes underlying this role are still poorly understood. This review focuses on the relationship between the intestinal bacterial microbiota and immune cells to determine how the commensal microbiome influences the initiation and development of CRC.

Antibiotic Resistance Determinants and Virulence Factors of Hypervirulent and Carbapenem Non-Susceptible Pseudomonas aeruginosa.

BACKGROUND: The aim was to investigate the distribution of antibiotic resistance determinants and virulence factors in a group of carbapenem non-susceptible Pseudomonas aeruginosa (P. aeruginosa). METHODS: From March 2018 to May 2019, a total of 98 P. aeruginosa samples were collected from 6 hospitals in Ningbo and Hangzhou, Zhejiang Province, China. Drug susceptibility tests to 13 antimicrobial agents were conducted. The presence of antibiotic resistance determinants and virulence factors were investigated by PCR, including 39 ß-lactamase genes, 14 aminoglycoside modifying enzyme genes, 10 16SrRNA methylase genes, and 11 virulence genes. Phylogenetics of 98 P. aeruginosa was analyzed by sample cluster analysis (UPGMA). RESULTS: PCR revealed the presence of 7 ß-lactamase genes, 5 aminoglycoside modifying enzymes, 1 16S rRNA methylase gene, and 8 virulence genes in total, at least 2 ß-lactamase genes and 4 virulence genes were positive in every isolate. In addition, regional differences in distributions of resistance and virulence genes remained between 2 cities. Sample cluster analysis showed that the strains had obvious aggregation and were divided into several clusters, strains in the same cluster were isolated from different hospitals, even from different cities. CONCLUSIONS: Carrying resistance genes blaPDC and blaOXA-50 group and virulence genes plcH, aprA, and algD were the important epidemiological characteristics of this group of P. aeruginosa. The present findings provide insights into the mechanisms of hypervirulence as well as resistance to ß-lactams and aminoglycosides. To the best of our knowledge, this is the first report of blaPDC, blaOXA-50, and aph(3')-XV in P. aeruginosa in China.

Investigation of Virulence Genes and Resistance Genes in a Group of Staphylococcus aureus Isolated in Yuhang, China.

BACKGROUND: To investigate the distribution of virulence genes and resistance genes in a group of Staphylococcus aureus (S. aureus). METHODS: From February 2013 to April 2014, a total of 39 strains of S. aureus were collected at Hangzhou Yuhang Hospital of Traditional Chinese Medicine, China. Drug sensitivity to 16 kinds of antimicrobial agents was performed by E-test method. A total of 94 virulence genes and 11 resistance genes, including qacA and bsa, were examined by PCR. All virulence and resistance genes were used as molecular markers to perform sample cluster analysis (UPGMA). RESULTS: At least one gene in every class of virulence genes were positive in strains of S. aureus: adherence, exoenzyme, host immune evasion, and toxin. Eleven virulence genes encoding adherence were positive: clfA, clfB, ebpS, fnbA, icaA, isdA, isdB, isdC, sdrC, sdrD, sdrE; 5 virulence genes encoding exoenzyme were positive: hysA, lip, splB, edinB, nuc; 2 virulence genes encoding host immune evasion were positive: cap5, cap8; 55 kinds of virulence genes encoding toxin were positive: hla, hlb, hlg-2, psm-mec, pvl, sea, seb, sec, sed, see, seg, sei, sek, sel, sem, sen, seo, seq, tst, set1, set2, set3, set4, set5, set6, set7, set8, set9, set10, set11, set12, set13, set14, set15, set16, set17, set18, set19, set20, set21, set22, set24, set25, set26, set30 , set31, set32, set33, set34, set35, set36, set38, set39, set40, lukE. In addition, 39 strains of S. aureus were 100.0% susceptible to quinupristin/dalfopristin, rifampin, vancomycin, tigecycline, and had some resistance rates to 12 other kinds of antimicrobial agents. Six resistance genes were positive: mecA (53.8%), aac6'/aph2" (33.3%), aph3'-III (12.8%), ant4'/ant44" (23.1%), qacA (30.8%), bsa (12.8%). Sample cluster analysis suggested that this group of S. aureus were divided into cluster A and B, and presented a clearly aggregation. CONCLUSIONS: A great number of virulence genes were positive in this group of S. aureus, contributing to colonization and survival in the host, evading the host immune system, delivering toxins to the host, and promoting pathogenicities. This group of S. aureus also had high resistance, carried some kinds of resistance genes, and had clustering. The implementation of disinfection measures should be strengthened to prevent the occurrence of nosocomial infection.

Distribution of sasX, pvl, and qacA/B genes in epidemic methicillin-resistant Staphylococcus aureus strains isolated from East China.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) is a major nosocomial pathogen. Various virulence and antiseptic-resistant factors increase the pathogenicity of MRSA strains and allow for increased infection rates. PURPOSE: The purpose of this study was to investigate the prevalence and distribution of virulence-associated and antiseptic-resistant genes from epidemic MRSA strains isolated from East China. METHODS: A newly designed multiplex PCR assay was used to assess whether the virulence-associated genes sasX and pvl and the chlorhexidine tolerance gene qacA/B were present in 189 clinical isolates of MRSA. Multilocus sequence typing (MLST) and Staphylococcal protein A (spa) typing of these isolates were also performed. The frequency of these genes in isolates with epidemic sequence types (STs) was investigated. RESULTS: Twenty STs and 36 spa types with five epidemic clones (ST5-t311, ST59-t437, ST5-t002, ST239-t030, and ST239-t037) were identified. The prevalence of sasX, pvl, and qacA/B in all isolates was 5.8%, 10.1%, and 20.1%, respectively. The prevalences of these genes in isolates with ST5, ST59, ST239, and other ST genetic backgrounds were all significantly different (P<0.001). Isolates that had the highest frequency of sasX, pvl, or qacA/B were ST239 (33.3%), ST59 (28.9%), and ST5 (34.1%), respectively. The gene distribution pattern from all of the isolates showed that sasX-pvl-qacA/B+, sasX-pvl+qacA/B-, and sasX+pvl-qacA/B- were closely associated with epidemic clones ST5-t311, ST59-t437, and ST239-t037, respectively. CONCLUSION: There are significant differences in the prevalence of virulence-associated and antiseptic-resistant genes in epidemic MRSA strains. Using this information, more effective control and prevention strategies for nosocomial MRSA infections can be developed.

[Emergence of novel variants of gyrA, parC, qnrS genes in multi-drug resistant Klebsiella caused pneumonia].

OBJECTIVE: To investigate the resistant mechanism of quinolones on multi-drug resistant Klebsiella caused pneumonia (MDR-KPN). METHODS: From August 2008 to May 2010, 47 strains of MDR-KPN were collected from 6 hospitals in Hangzhou and Huzhou in Zhejiang province in China. Drug target genes to quinolones (gyrA, parC) and quinolone-resistance genes mediated by mobile genetic elements [qnrA, qnrB, qnrS, aac (6')-Ib-cr, qepA] were analyzed by PCR and verified by DNA sequencing. RESULTS: Positive results were found in 47 strains of MDR-KPN, 43 strains (91.5%) of gyrA mutation, 40 strains (85.1%) of parC mutation, 3 strains (6.4%) of qnrB2, 1 strain (2.1%) of qnrB 4, 8 strains (17.0%) of qnrS 1, 5 strains (10.6%) of qnrS 4, 2 strains (4.3%) of aac (6')-Ib-cr respectively. Moreover, 5 novel variants of gyrA (GenBank accession number: JN811952, JN811953, JN811954, JN811955, JN811956), 5 novel variants of parC (GenBank accession number: JN817432, JN817433, JN817434, JN817435, JN817436) were also identified. In addition, qnrS4 (GenBank accession number: JN836269) appeared to be the novel variants of qnrS. CONCLUSION: Quinolone-resistance-determining region played a key role on the resistance to quinolones in this group of MDR-KPN, and quinolone-resistance genes mediated by mobile genetic elements [qnrB2, qnrB4, qnrS1, qnrS4, aac (6')-Ib-cr] showed positive in some parts of the strains. This was the first report on emergence of qnrS4 in the world.