Journal of Cellular Immunology

The gut microbiome or gut flora is a vast community of microorganisms such as bacteria, viruses, protozoa, and fungi that inhabit the digestive tract of the human and other animals [1,2]. In the human body, bacterial species colonize into the oral cavity, skin, vagina, and placenta, however, the largest population of microorganisms resides in the intestine.

When immune cells are activated, they undergo metabolic change in order to have sufficient energy to function effectively. The Krebs cycle is one of the most important pathways involved in this response and citrate, a critical component of this pathway, regulates carbohydrate and lipid metabolism.

The important immune cells in the brain are called microglia acting as the central junction between neuroinflammation and neurodegenerative diseases. In patients of cognitive disorders and Alzheimer’s disease (AD) animal models, amoebic morphology and inflammatory pathways are activated to release numerous cells in the inflammatory factors by active microglia.

Inflammation can be caused by various environmental factors, including microbial infection and toxic chemical exposure. In response to inflammation, immune cells like macrophages, B and T lymphocytes, fibroblasts, endothelial cells, and various stromal cells secrete soluble polypeptide cytokine Tumor Necrosis Factor Alpha (TNF?)

The exchange of information within the cell is extremely complex. Besides the well-studied chemical signalling, physical signalling is required to fulfil spatial and temporal aspects. The Golgi apparatus and the microtubule skeleton system are the decisive structures for numerous intracellular transport tasks.

Inhaled budesonide benefits patients with COVID-19. ProLung™-budesonide enables the sustained, low dose administration of budesonide within a delivery vehicle similar to lung surfactant.

Acute respiratory distress syndrome (ARDS) is the major cause of mortality among hospitalized acute lung injury (ALI) patients. Lung macrophages play an important role in maintaining the tissue-fluid homeostasis following injury. We recently showed that circulating monocytes recruited into the alveolar space suppressed the stimulator of type 1 interferon genes (STING) signaling in alveolar macrophages through sphingosine-1-phosphate (S1P). 

The immune system is essential to host defense because it senses attacking pathogens and elicits protective immune responses. Although immune responses can protect against pathogens, uncontrolled immune responses cause tissue damage and other pathological consequences through their inflammatory mediators. 

Tumor-derived small extracellular vesicles or exosomes which carry the checkpoint PD-L1 are directly involved in immune evasion and uncontrolled tumor growth. We have recently reported that PD-L1 is also enriched on Wharton’s Jelly Mesenchymal Stromal Cell (WJMSC)-associated exosomes.

AD is a neurodegenerative disease characterized by progressive cognitive impairment, behavioral changes, memory loss and executive dysfunction, all of which present serious threats to the health of older people.

Traumatic brain injury (TBI) has a bimodal age distribution with peak incidence at age 24 and age 65 with worse outcomes developing in aged populations

Effector CD4⁺ T cells (i.e. Th1, Th2, Th17) are essential in the adaptive immune system’s specific elimination of different classes of pathogens, such as viruses, bacteria, and parasites, while regulatory T cells shut these inflammatory responses off once a pathogen has been cleared [1]. Interestingly, effector T cells preferentially utilize

The balance between cell removal following tissue damage and new cell formation to facilitate repair has long been linked to the behaviour of inflammatory macrophages and their interactions with tissue-resident non-immune cells. The main aim of the inflammatory response is to modulate the tissue environment by removing unwanted cells and recruiting cells and soluble factors from the bloodstream to help protect the damaged tissue against infective foreign bodies.

Extracellular vesicles (EVs) are emerging as a key mediator of intercellular communication as well as a major mechanism of functional reprogramming of cells in disease. All cells produce EVs, which freely circulate and are found in all body fluids. EVs are heterogenous, consisting of subsets of vesicles with different sizes, distinct origins, and various functions (Figure 1). They mediate a broad variety of biological events ranging from cellular activation, inflammation, blood coagulation, angiogenesis, cellular transport, and others. Among these vesicles, a subset of small EVs (30-150 nm in diameter) originating from multivesicular bodies (MVBs) in parent cells and referred to as small extracellular vesicles (sEVs) carry proteomic, genomic and functional signatures that resemble those of parent cells and are, therefore, taken as surrogates of parent cells. In cancer, tumor-derived exosomes (TEX) reflect characteristics of tumor cells and are considered candidates for “liquid tumor biopsy”. Emerging evidence shows that TEX are a major sEV subset in plasma of patients with cancer, including hematologic malignancies.

Current research investigating the pathomechanisms of neurodegenerative disorders of the central nervous system (CNS), such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), or Parkinson’s disease (PD), led to the understanding that these diseases have to be seen in the context of immune responses [1]. In other words,

The western diet and overuse of anti-inflammatory medication have caused a great deal of stress on the liver. Obesity and the associated inflammatory state in insulin-responsive tissues result in the release of pro-inflammatory cytokine that activates the stress-responsive MAPKs, p38 MAPK, and JNK. These MAPKs have figured prominently as critical effectors in physiological and pathophysiological hepatic inflammation.

The mammalian gut is the largest organ of adaptive immune responses with a total surface area of 300 m2 of the gut epithelium. The intestinal mucosa contains at least 80% of the body’s activated B cells.

ZBP1 has aroused a wide interest since it was identified as the first cytosolic dsDNA sensor ahead of the finding of cGAS in 2013. However, the investigations on ZBP1 declined when researchers found the binding of ZBP1 with dsDNA is not absolutely required for the activation of innate response.

We reviewed the anti-tumor mechanisms of short-chain fatty acids (SCFAs) as well as the relationship between the gut microbiome and the pathology of colorectal carcinoma (CRC). According to our in silico analysis of human CRC cell lines, it was shown that SCFAs suppress various genes and transcription factors that participate in tumor growth/proliferation and cell turnover, and butyric acid displayed the strongest inhibitory effects among SCFAs.

Recently researchers have focused on the role of neuroinflammation in neurodegenerative diseases such as Alzheimer’s disease, atrophic lateral sclerosis, Huntington’s disease, Multiple sclerosis and Parkinson’s disease (PD). PD is one of the leading neurodegenerative diseases in developed countries and the complete etiological scenario remains unknown. A-synuclein misfolding and aggregation, mitochondrial dysfunction, dysfunctional protein clearance and ubiquitin/proteasome systems, and neuroinflammation have been associated with PD.