Combined with human-to-human contact, the potential for SARS-CoV-2 virus transmission via aerosols and feces raises the urgency for effective treatment of hospital wastewater (HWW), which has been assumed as an important source of pathogenic microorganisms spreading into aquatic environments. However, there are few reviews discussing the presence and removal of pathogens in hospital wastewaters matrices. This review summarizes the pathogenic microorganisms including bacteria, fungi, viruses and parasites present in hospital wastewater, the related diseases and treatment processes. In addition, the removal of pathogens during hospital wastewater treatment process is reviewed, including the preliminary process, secondary process and tertiary process. Due to the growing concerns over the effects of the current global pandemic on hospital wastewater treatment process, further research is necessary to investigate the actual fate of pathogens in hospital wastewater and optimize disinfection processes.

Streptococcus suis serotype 2 (SS2) is an emerging human pathogen worldwide. A large outbreak occurred in the summer of 2005 in China. Serum samples from this outbreak revealed that levels of the main proinflammatory cytokines were significantly higher in patients with streptococcal toxic-shock-like syndrome (STSLS) than in patients with meningitis only. However, the mechanism underlying the cytokine storm in STSLS caused by SS2 remained unclear. In this study, we found that suilysin (SLY) is the main protein inflammatory stimulus of SS2 and that native SLY (nSLY) stimulated cytokines independently of its haemolytic ability. Interestingly, a small amount of SLY (Å Mol/L) induced strong, long-term TNF-α release from human PBMCs. We also found that nSLY stimulated TNF-α in wild-type macrophages but not in macrophages from mice that carried a spontaneous mutation in TLR4 (P712H). We demonstrated for the first time that SLY stimulates immune cells through TLR4. In addition, the Myd88 adaptor-p38-MAPK pathway was involved in this process. The present study suggested that the TLR4-dependent inflammatory responses induced by SLY in host might contribute to the STSLS caused by SS2 and that p38-MAPK could be used as a target to control the release of excess TNF-α induced by SS2.

As a specialized subset of intestinal epithelial cells (IECs), goblet cells (GCs) play an important role during the antibacterial response via mucin production. However, the regulatory mechanisms involved in GC differentiation and function during infection, particularly the role of immune cell–IEC cross-talk, remain largely unknown. In this study, using Villin^∆Ltbr conditional knockout mice, we demonstrate that LTβR, expressed on IECs, is required for GC hyperplasia and mucin 2 (MUC2) expression during Listeria infection for host defense but not homeostatic maintenance in the naive state. Analysis of single gene-deficient mice revealed that the ligand lymphotoxin (LT), but not LIGHT, and type 3 innate lymphoid cells (ILC3s), but not conventional T cells, are required for MUC2-dependent Listeria control. Conditional deficiency of LT in ILC3s further confirmed the importance of LT signals derived from ILC3s. Lack of ILC3-derived LT or IEC-derived LTβR resulted in the defective expression of genes related to GC differentiation but was not correlated with IEC proliferation and cell death, which were found to be normal by Ki-67 and Annexin V staining. In addition, the alternative NF-κB signaling pathway (involving RelB) in IECs was found to be required for the expression of GC differentiation-related genes and Muc2 and required for the anti-Listeria response. Therefore, our data together suggest a previously unrecognized ILC3–IEC interaction and LT–LTβR–RelB signaling axis governing GC differentiation and function during Listeria infection for host defense. Key Points ILC3-derived LT and IEC-derived LTβR regulate innate defense against Listeria. LT–LTβR axis increases GC numbers and MUC2 expression during Listeria infection. LTβR signaling and downstream RelB are associated with GC differentiation.

With the rapid development of clinical diagnosis and treatment, many traditional and conventional in vitro diagnosis technologies are unable to meet the demands of clinical medicine development. In this situation, nanomaterials are rapidly developing and widely used in the field of in vitro diagnosis. Nanomaterials have distinct size-dependent physical or chemical properties, and their optical, magnetic, electrical, thermal, and biological properties can be modulated at the nanoscale by changing their size, shape, chemical composition, and surface functional groups, particularly because they have a larger specific surface area than macromaterials. They provide an amount of space to modify different molecules on their surface, allowing them to detect small substances, nucleic acids, proteins, and microorganisms. Combining nanomaterials with in vitro diagnosis is expected to result in lower detection limits, higher sensitivity, and stronger selectivity. In this review, we will discuss the classfication and properties of some common nanomaterials, as well as their applications in protein, nucleic acids, and other aspect detection and analysis for in vitro diagnosis, especially on aging-related nanodiagnostics. Finally, it is summarized with guidelines for in vitro diagnosis.

Listeria monocytogenes (Lm) is a facultative, intracellular Gram-positive pathogenic bacterium that causes sepsis, a condition characterized by persistent excessive inflammation and organ dysfunction. However, the pathogenesis of Lm-induced sepsis is unknown. In this research, we discovered that TRIM32 is required for innate immune regulation during Lm infection. Trim32 deficiency remarkably reduced bacteremia and proinflammatory cytokine secretion in mice with severe Lm infection, preventing sepsis. Trim32^−/− mice had a lower bacterial burden after Lm infection and survived significantly longer than wild-type (WT) mice, as well as lower serum levels of inflammatory cytokines TNF-α, IL-6, IL-18, IL-12p70, IFN-β, and IFN-γ at 1 day post infection (dpi) compared to WT mice. On the other hand, the chemokines CXCL1, CCL2, CCL7, and CCL5 were enhanced at 3 dpi in Trim32^−/− mice than WT mice, reflecting increased recruitment of neutrophils and macrophages. Furthermore, Trim32^−/− mice had higher levels of macrophage-associated iNOS to kill Lm. Collectively, our findings suggest that TRIM32 reduces innate immune cells recruitment and Lm killing capabilities via iNOS production. Graphical Abstract

Pregnant women are at a high risk of contracting listeriosis; however, there have been only a few clinical reports of maternal bacteremia occurring before 20 weeks of gestation in China. In this case report, a 28-year-old pregnant woman at 16 weeks and 4 days of gestation was admitted to our hospital suffering from fever for four days. The patient was initially diagnosed with an upper respiratory tract infection at the local community hospital; nevertheless, the cause of the infection was unknown. In our hospital, she was diagnosed with Listeria monocytogenes (L. monocytogenes) infection by the blood culture system. Before the results of blood culture were obtained, ceftriaxone and cefazolin were given for three days respectively based on clinical experience. However, the fever didn't reduce until she was treated with ampicillin. This pathogen was further identified as L. monocytogenes ST87 by serotyping, multilocus sequence typing (MLST), and virulence gene amplification. Finally, a healthy baby boy was born in our hospital, and the neonate was developing well at the 6-week postnatal follow-up visit. This case report suggests that patients with L. monocytogenes ST87-caused maternal listeriosis can have a good prognosis; however, more clinical information and molecular experiments are needed to confirm our hypothesis.