Evaluation of Th2 and Th17 Immunity-Related Factors as Indicators of Brucellosis

Abstract

ObjectiveBrucellosis is a common bacterial zoonotic infection, and greater than half a million new cases are diagnosed annually. This study investigates the expression of Th2 and Th17 immunity-related factors (Th2-LCR lncRNA, IL-25, TRAF3IP2, and IL-17RB) in different stages of Brucella infections.Material and MethodsIn total, 99 brucellosis patients were divided into three groups (acute = first infection before treatment, relapse = before treatment, and treated = after treatment for 6–8 weeks with doxycycline and rifampin). Thirty-three healthy volunteers represented the control group. Gene expression levels were assessed by quantitative amplification in reference to the 18S rRNA gene and statistically evaluated.ResultsNo significant differences in the expression of these genes were observed between the control group and patients after completion of antibiotic treatment. Compared to these two groups, only Th2-LCR lncRNA and TRAF3IP2 were significantly more highly expressed in the acute group. Th2-LCR lncRNA was also significantly elevated in the relapse group. TRAF3IP2 expression was additionally significantly increased in the acute group compared to the relapse group.ConclusionIL-25 and IL-17RB failed to differentiate between the infected and noninfected groups. TRAF3IP2 and Th2-LCR lncRNA might be good indicators of brucellosis during the acute phase, but the expression levels varied strongly among patients. To verify the suitability of these factors as an indicator for brucellosis, acute infection or relapse should be investigated in further studies on larger cohorts with well-defined inclusion criteria.

Ninety-six–hour starved peripheral blood mononuclear cell supernatant inhibited LA7 breast cancer stem cells induced tumor via reduction in angiogenesis and alternations in Gch1 and Spr expressions

“…The control group was used to normalize and compare the changes in the expression levels of the targets between the groups. To calculate gene expression level, 2 -△△Ct formula was hired for all target genes (Figure 7) (35). The expression level of Spr gene in 96 h-SPS-treated LA7induced tumors was significantly decreased compared with RPMI or normal saline treated groups (Figure 7A, p< 0.05).…”

Exploring secretory proteome and cytokine kinetic of human peripheral blood mononuclear cells exposed to methicillin-resistant Staphylococcus aureus biofilms and planktonic bacteria

“…The immune response against bacteria in chronic infections is complex and involves both the innate and adaptive immune systems (9,10). The innate immune response is the first line of defense and is activated by the pattern recognition receptor (PRR) pathways that detect general but bacterial-specific markers such as lipoproteins, peptidoglycans, and their breakdown products, or unmethylated CpG motifs in the DNA by different specialized Toll-like receptor (TLR) (11)(12)(13). This leads to the activation of phagocytic cells, such as macrophages and neutrophils, and the production of proinflammatory cytokines, such as IL-1, IL-6, IL-12p70, IL-18, and TNF, by host innate immune cells, including monocytes.…”

Brucella Phagocytosis Mediated by Pathogen-Host Interactions and Their Intracellular Survival

“…The causative agent, Brucella species, is a Gram-negative facultative intracellular bacterium. Among Brucella species, three of them are known to be endemic in most countries and are highly virulent to both their natural hosts and to humans, including B. abortus, B. melitensis and B. suis that primarily infect cattle, sheep and goats, and domestic feral and wild swine populations, respectively [ 4 , 9 ]. Brucella lacks well-known or classical virulence factors such as spores, fimbriae, cytolysins, exotoxins, secreted proteases, antigenic variation, resistance forms, phage-encoded toxins, virulence plasmids, and capsules [ 7 , 10 ].…”

“…The virulence factors that have been reported to be necessary for invasion, the establishment of infection, as well as intracellular survival and replication of Brucella are cyclic β-1,2-glucan (CβG), VirB T4SS, pathogen-associated molecular patterns, two-component sensory and regulatory system BvrS/BvrR, and lipopolysaccharide (LPS) [ 2 , 7 ]. Brucella LPS is altered, so it is a weak inducer of the host inflammatory response compared to LPS molecules of other Gram-negative bacteria [ 9 , 11 ]. Other virulence factors include outer membrane proteins, BacA, SagA, BmaC, BetB, BtaE, MucR, and a genomic island associated with Brucella pathogenicity [ 7 ].…”