Interleukin (IL)-33 is a critical regulator of allergic airway inflammation in the lung and is released by stressed or damaged epithelial cells. Here, Applicants show that alveolar macrophages regulate epithelial alarmin expression via CLEC-2 (C-type Lectin-like Receptor-2), which binds to PDPN (podoplanin). Therefore, CLEC-2/PDPN interactions are critical for regulating type 2 immunity in the lung and modulating expression of the epithelial alarmin IL-33. Methods are disclosed for therapeutic and screening applications. Novel therapeutic targets in alveolar macrophages and epithelial cells are disclosed.

The current disclosure provides use of high dose nicotinamide adenine dinucleotide (NAD) precursor regimens for reduction of inflammation in human patients with preexisting inflammation. The NAD precursor can be nicotinamide riboside (NR) and the high dose regimen can include at least 1000 or 2000 mg/day for at least 9 days.

The invention relates to a method for detecting contaminants of glucose polymers, said contaminants being capable of acting in synergy with one another so as to trigger an inflammatory reaction, characterized in that it comprises an in vitro inflammatory response test using modified cell lines.

This invention is directed to the treatment of cancer, particularly solid tumors, using cabozantinib in combination with an immune checkpoint inhibitor or an anti-cancer vaccine and in predicting responses to such cancer treatments.

The present disclosure relates to the use of a compound of formula (I) ##STR00001##
or anyone of its pharmaceutically acceptable salts, in the treatment and/or prevention of an inflammatory disease; wherein: ##STR00002##
means an aromatic ring wherein V is C or N and when V is N; Q is N or O, provided that R″ does not exist when Q is O; R′ independently represent a hydrogen atom or a group chosen among a (C.sub.1-C.sub.3)alkyl group, a halogen atom, a hydroxyl group, a —COOR.sub.1 group, a —NO.sub.2 group, a —NR.sub.1R.sub.2 group, a morpholinyl or a morpholino group, a N-methylpiperazinyl group, a (C.sub.1-C.sub.3)fluoroalkyl group, a —O—P(═O)—(OR.sub.3)(OR.sub.4) group, a (C.sub.1-C.sub.4)alkoxy group and a —CN group, and can further be a group chosen among: ##STR00003##

An empirical Screen for Anti-infectives using Fluorescence microscopy of IntracellulaR Enterobacteriaceae (SAFIRE) was developed. Using this methodology, a library of small molecules and identified antimicrobials that are cell permeable and non-host-toxic were screened. Inhibitors of bacterial efflux pumps were identified as being implicated in antibiotic resistance and are attractive therapeutic targets for antimicrobials.

The present disclosure relates to the use of a compound of formula (I) ##STR00001##
or anyone of its pharmaceutically acceptable salts, in the treatment and/or prevention of an inflammatory disease; wherein: ##STR00002##
means an aromatic ring wherein V is C or N and when V is N; Q is N or O, provided that R″ does not exist when Q is O; R′ independently represent a hydrogen atom or a group chosen among a (C.sub.1-C.sub.3)alkyl group, a halogen atom, a hydroxyl group, a —COOR.sub.1 group, a —NO.sub.2 group, a —NR.sub.1R.sub.2 group, a morpholinyl or a morpholino group, a N-methylpiperazinyl group, a (C.sub.1-C.sub.3)fluoroalkyl group, a —O—P(═O)—(OR.sub.3)(OR.sub.4) group, a (C.sub.1-C.sub.4)alkoxy group and a —CN group, and can further be a group chosen among: ##STR00003##

The present disclosure provides an in vitro method of generating bovine monocyte-derived macrophages from monocytes that produce nitric oxide and use as an indicator of innate immune response potential. The culture system includes culturing bovine monocytes in serum-free media supplemented with granulocyte-macrophage stimulating factor (GM-CSF) to generate monocyte-derived macrophages that produce nitric oxide.

Disclosed are methods of modulating macrophage activation to treat various diseases, such as cancer, fibrosis, infectious diseases, inflammatory diseases, metabolic diseases, or autoimmune diseases. Also disclosed are methods of identifying compounds useful for modulating macrophage activation as means to treat cancer, fibrosis, infectious diseases, inflammatory diseases, metabolic diseases, or autoimmune diseases.

Aspects of the present disclosure include methods for modulating macrophage activity. Methods according to certain embodiments include contacting a macrophage with a mannose receptor (CD206) binding agent in a manner sufficient to modulate activity of the macrophage. Methods for converting a phenotype of a macrophage from an M2 phenotype to an M1 phenotype are also provided. Methods for inhibiting growth of a CD206-expressing cell as well as methods for treating a subject for a neoplastic condition (e.g., cancer) or a condition associated with chronic inflammation are described. Immuno-modulating peptides suitable for use in the subject methods are also presented.