BACKGROUND: Keratinocyte dysdifferentiation and proinflammatory cytokine production play a central role in psoriatic inflammation. According to recent studies, the Rh family C glycoprotein (RHCG) enhances cell proliferation and disrupts cell differentiation. However, the specific role of RHCG psoriasis development remains unclear.
OBJECTIVE: We here explored the effect of RHCG on keratinocytes under psoriatic inflammation.
METHODS: The cell counting kit‑8 assay was conducted to assess proliferation. RHCG protein expression was assessed through western blotting and enzyme-linked immunosorbent assays. The expression of proinflammatory cytokines and differentiation markers was analyzed through a quantitative reverse-transcription polymerase chain reaction.
RESULTS: Both RHCG mRNA and protein levels increased in psoriatic skin. Notably, cultured keratinocytes treated with an M5 cocktail, which mimics psoriatic inflammation, exhibited higher RHCG expression. Furthermore, RHCG overexpression promoted keratinocyte proliferation, accompanied by an increase in the production of interleukin (IL)-1β, IL-6, and IL-8, and tumor necrosis factor-α. RHCG overexpression also resulted in higher expression of keratin 17, a differentiation marker. Conversely, RHCG gene knockdown reduced keratinocyte proliferation and cytokine secretion. RHCG inhibition in cells recovered both keratin 1 and loricrin expression. Additionally, RHCG overexpression facilitated the phosphorylation of nuclear factor-kappa B and extracellular signal-regulated protein kinase signaling pathways. Importantly, when these signaling pathways were inhibited, the effect of RHCG on keratinocytes was attenuated.
CONCLUSIONS: These findings support the substantial role of RHCG in psoriatic inflammation development and suggest that RHCG serves as a potential target for psoriasis treatment.

The characteristics of cytokine/chemokine(CK) profiles across different courses of chronic hepatitis B virus infection and the effects of NAs antiviral therapy on cytokine profiles remain unclear.
This report provides evidence from 383 patients with chronic HBV infection. The Luminex multiple cytokine detection technology was used to detect CK profiles. The predictive power of CKs across course of disease was assessedusing univariate analyses and with receiver operating characteristic (ROC) curves.
Compared to healthy control (HC), expression levels of interleukin 6 (IL)-6, IL-8, IL-21, matrix metalloproteinases (MMP)-2 and tumor necrosis factor receptor (TNFR)-1 showed a significant increasing trend during chronic HBV infection. IL-23 and IL-33 increased respectively in chronic hepatitis B patients (CHB). interferon (IFN)-gamma and TNF-α changed significantly only in liver cirrhosis (LC) patients. Whereas, myeloid-related markers decreased dramatically in those with hepatocellular carcinoma (HCC). The ROC result suggests that combining IL-6, IL-8, CXCL9 and CXCL13 into a nomogram has closely correlation with HCC during chronic HBV infection. In addition, nucleotide analogues (NAs) antiviral treatments are capable of recoveringnormal liver functions and significantly reducing the viral loads, however, they seem to have a limited effect in changing CKs, especially specific antiviral factors.
The differential CK and virological markers may serve as potential indicators of distinct immune statuses in chronic HBV infection. They also underscore the varying efficacy and limitations of NAs antiviral therapies. This next step would to break new ground in the optimization of current anti-HBV treatment programs although this requires further research.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by neutrophils airway infiltration. It is currently known that Interleukin-17 (IL-17) is an important pro-inflammatory factor. It can promote the accumulation of neutrophils and participate in the chronic inflammatory process of COPD. However, the value of IL-17 levels in the diagnosis and assessment of COPD remains controversial. In view of this, we conducted a systematic review and meta-analysis to assess its relevance.
We searched databases such as PubMed, Web of Science, Cochrane Library and Embase to extract original research.
A total of 10 studies with 2268 participants were included in this meta-analysis. The results showed that the level of serum IL-17 in patients with stable COPD was significantly higher than that in healthy controls (standard mean difference SMD, 1.59, 95% CI 0.84-2.34; p<0.001). Compared with the stable COPD group, the serum IL-17 level in acute exacerbation (AECOPD) was significantly higher (SMD, 1.78, 95% CI 1.22-2.33; p<0.001). The level of IL-17 in sputum of COPD patients was also higher than that of healthy controls (SMD, 2.03, 95% CI 0.74-3.31; p<0.001).
Our results showed that IL-17 levels were elevated in serum and sputum in COPD patients compared with healthy controls, and IL-17 levels increased with disease progression. IL-17 serves as a potential biomarker to indicate the persistence of neutrophilic inflammation and exacerbation of COPD.

This article aims to analyze the effects of enzyme treatment concentration, temperature, and time on peanut protein so as to obtain an optimal enzymatic hydrolysis condition for flavorzyme (Fla) and alkaline protease (Alk). The results were as follows: enzymatic hydrolysis temperature 60 °C and 55 °C, enzyme concentration 10% and 4%, enzymatic hydrolysis time 80 min and 60 min, and double enzyme hydrolysis ratio 2% Fla + 5% Alk, respectively. The BALB/c mice were sensitized with gavage of peanut protein before and after enzyme treatment to evaluate the effects of different enzyme treatments on peanut allergenicity. Compared with the mice sensitized with raw peanuts, the weight growth rate of the mice sensitized with enzyme treatment peanut increased but not as much as the control, the degranulation degree of mast cell and basophils decreased, the inflammatory infiltration and congestion in jejunum and lung tissue decreased, the expression of proinflammatory factors and thymic stromal lymphopoietin (TSLP) gene decreased, and the secretion of specific antibodies (IgE, and IgG) decreased, and the binding ability of peanut protein with peanut-specific IgE antibodies decreased as well. The results above indicate that the allergenicity of peanut protein decreases after enzyme treatment and the dual enzyme (Fla + Alk) treatment can be much more efficient.

[This corrects the article DOI: 10.3389/fcimb.2022.1022857.].

The objective of this study was to investigate whether dietary supplementation with benzoic acid, Enterococcus faecium, and essential oil complex (BEC) could help laying hens recover from coccidia and Clostridium perfringens type A challenge. A total of 60 (35-wk-old) Lohmann-laying hens were randomly assigned to 3 experimental groups (10 replicates with 2 hens per replicate): I) control group (CON), II) challenge group (CC), and III) BEC group (2,000 mg/kg BEC). The total experimental period was 8 wk. The results shown that the challenge layers had lower egg-laying rate and average daily feed intake (ADFI) (P < 0.05), and addition of BEC after challenge increased egg-laying rate (P < 0.05). The content of propionic acid (PA) and butyric acid (BA) in short-chain fatty acid (SCFA) was significantly decreased by challenge (P < 0.05). CC and BEC groups had lower villus height to crypt depth ratio (V/C) and higher pathological scores in duodenum (P < 0.05), whereas the BEC group had lower pathological scores in jejunum when compared with the CC group (P < 0.05). The challenge increased the concentration of proinflammatory cytokines (IL-1β and IL-6) (P < 0.05). An increase in the abundance of Bacteroidoes (genus), Bacteroidaceae (family), Bacteroidoes sp. Marseille P3166 (species), Bacteroidoes caecicola (species) was observed in the CC group, whereas the BEC group had higher abundance of Bacteroides caecigallinarum (species). The genera Faecalibacterium and Asterolplasma were positively correlated with egg-laying rate (r = 0.57, 0.60; P < 0.01); and the genera Bacteroides and Romboutsia were negatively correlated with egg-laying rate (r = -0.58, -0.74; P < 0.01). The genera Bacteroides, Lactobacillus, and Rombutzia were positively correlated with jejunal mucosa proinflammatory factor IL-1β level (r = 0.61, 0.60, 0.59; P < 0.01), which were negatively correlated with genera Rikenbacteriaceae RC9, Faecalibacterium, and Olsenlla (r = -0.56, -0.57, -0.61; P < 0.01). There genera UCG.005 was positively correlated with proinflammatory factor IL-6 level in jejunal mucosa (r = 0.58; P < 0.01), which was negatively correlated with Rikenbacteriaceae RC9 (r = -0.62; P < 0.01). The experiment results revealed that the addition of BEC to the diet restored the production performance of the laying hens. In addition, supplementation of 2,000 mg/kg BEC modulated gut health by reducing gut damage scores and modulating microbial composition, thereby promoting recovery of laying hens after coccidia and Clostridium perfringens challenge.

To compare the difference of gut microbiota between preeclampsia (PE) and healthy normal pregnant women, providing new therapeutic strategy for preeclampsia.
Forty-one PE patients and 45 age- and pre-pregnancy body mass index- matched healthy controls were enrolled from Nov 2021 to May 2022 in this retrospective case-control study. Fecal microbiota was detected by 16S rRNA gene sequencing, followed by bioinformatics analysis including microbial α diversity, microbial β diversity, and linear discriminant analysis effect size (LEfSe) analysis. Serum inflammatory factors were also detected and compared between the two groups.
There were significant differences in Bacteroidetes (2.68% in PE patients vs 11.04% in healthy controls, P < 0.001), Proteobacteria (4.04% in PE patients vs 1.22% in healthy controls, P = 0.041), and Fusobacteria (1.07% in PE patients vs 0.01% in healthy controls, P = 0.042) between the two groups at the phylum level. Microbial α diversity was lower in PE patients than that in healthy controls. In addition, there was significant difference in microbial β diversity between the two groups. LEfSe analysis showed that there are 24 different taxa between the two groups. The levels of proinflammatory factors including serum tumor necrosis factor-α and Interleukin-6 were statistically significant higher in PE patients than those in healthy controls (both P < 0.001), while there were no significant differences in the levels of serum anti-inflammatory factors including Interleukin-4 and Interleukin-10 between the two groups (P = 0.234 and P = 0.096, respectively).
PE patients demonstrated gut microbiota disturbances and increasing serum proinflammatory factors, leading to a better understanding of the relationship between the gut microbiota dysbiosis and PE.

Acute kidney injury (AKI) is a complex clinical syndrome with multiple etiologies and pathogenesis, which lacks early biomarkers and targeted therapy. Recently, macrophage migration inhibitory factor (MIF) family protein have received increasing attention owing to its pleiotropic protein molecule character in acute kidney injury, where it performed a dual role in the pathological process. macrophage migration inhibitory factor and macrophage migration inhibitory factor-2 are released into the peripheral circulation when Acute kidney injury occurs and interact with various cellular pathways. On the one hand, macrophage migration inhibitory factor exerts a protective effect in anti-oxidation and macrophage migration inhibitory factor-2 promotes cell proliferation and ameliorates renal fibrosis. On the other hand, macrophage migration inhibitory factor aggravates renal injury as an upstream inflammation factor. Herein, we provide an overview on the biological role and possible mechanisms of macrophage migration inhibitory factor and macrophage migration inhibitory factor-2 in the process of Acute kidney injury and the clinical application prospects of macrophage migration inhibitory factor family proteins as a potential therapeutic target.

Helicobacter pylori is a Gram-negative, spiral-shaped bacillus that colonizes 50% of the world population and is considered a class 1 carcinogen by the World Health Organization. This pathogen is the most common cause of infection-related cancers. Apart from cancer, it also causes several gastric and extra gastric diseases. Eradication of H. pylori using antibiotics is a global challenge because of its drug resistance. Alternative treatment options are gaining more attention to tackle drug-resistant H. pylori infections. Several medicinal plants and their isolated compounds have been reported for their antimicrobial activity against H. pylori. The mechanism of action of many of these plant extracts and plant-derived compounds is different from that of conventional antibiotics. Therefore they are shown to be effective against drug-resistant strains of H. pylori. They act by inhibiting bacterial enzymes, adhesions with gastric mucosa, suppression of nuclear factor-κB and by inhibition of oxidative stress. Extracts from Pistacia lentiscus, Brassica oleracea, Glycyrrhiza glabra, Camellia sinensis, Cinnamomum cassia, Allium sativum and Nigella sativa plants and isolated phyto-compounds such as curcumin, resveratrol, quercetin, allicin and ellagic acid demonstrated antimicrobial activity against H. pylori under in vivo conditions. The plant extracts of Zingiber officinale, Glycyrrhiza glabra; and phytochemical allicin and berberine when combined with standard treatment, result in a dramatic increase in H. pylori eradication. In this review, we highlighted the therapeutic efficacy of different plant extracts and isolated phyto compounds against H. pylori infection and described their role in tackling H. pylori resistance to antibiotics.

Hypertension is a severe public health problem that induces cardiac injury with alterations of gene expressions. The current study sought to evaluate the mechanism of microRNA(miR)-135a-5p in NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediation of cardiac inflammation and hypertensive cardiac fibrosis. Firstly, hypertensive mouse models were established using angiotensin II (Ang II), followed by miR-135a-5p agomir treatment. Subsequently, mouse blood pressure and basic cardiac function indexes, histopathological changes, and cardiac fibrosis were all determined, in addition to detection of factors related to inflammation and fibrosis. Additionally, mice cardiac fibroblasts (CFs) were isolated and treated with Ang II. The binding relationship of miR-135a-5p and thioredoxin-interacting protein (TXNIP) was predicted and testified, while the interaction of TXNIP and NLRP3 was detected by means of a co-immunoprecipitation assay. It was found that miR-135a-5p was poorly-expressed in Ang II-treated mice and further exerted cardioprotective effects against hypertensive heart diseases. Moreover, over-expression of miR-135a-5p resulted in inhibition of inflammatory infiltration and almost eliminated cardiac fibrosis, as evidenced by decreased Collagen (COL)-I, COL-III, a-smooth muscle actin, NLRP3, tumor necrosis factor-α, and interleukin-6. Mechanically, miR-135a-5p inhibited TXNIP expression to block the binding of TXNIP and NLRP3. On the other hand, TXNIP up-regulation reversed the protective role of miR-135a-5p over-expression in CFs. Collectively, our findings indicated that miR-135a-5p over-expression inhibited TXNIP expression to block the binding of TXNIP and NLRP3, thereby alleviating hypertensive cardiac inflammation and fibrosis.