Transfusion of blood cell components is frequent in the therapeutic arsenal; it is globally safe or even very safe. At present, residual clinical manifestations are principally inflammatory in nature. If some rare clinical hazards manifest as acute inflammation symptoms of various origin, most of them linked with conflicting and undesirable biological material accompanying the therapeutic component (infectious pathogen, pathogenic antibody, unwanted antigen, or allergen), the general feature is subtler and less visible, and essentially consists of alloimmunization or febrile non-hemolytic transfusion reaction. The present essay aims to present updates in hematology and immunology that help understand how, when, and why subclinical inflammation underlies alloimmunization and circumstances characteristic of red blood cells and – even more frequently – platelets that contribute inflammatory mediators. Modern transfusion medicine makes sustained efforts to limit such inflammatory hazards; efforts can be successful only if one has a clear view of each element’s role.

• allergy
• alloimmunization
• blood components
• erythrocytes
• inflammation
• leukocytes
• platelets
• transfusion

• Cluster Analysis
• Cohort Studies
• Humans
• Inflammatory Bowel Diseases/etiology
• Inflammatory Bowel Diseases/microbiology
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology
• Metagenome
• Microbiota
• Phenotype
• RNA, Ribosomal, 16S

• UL1TR000124 NCATS NIH HHS
• U01 DK062413 NIDDK NIH HHS
• HG005964 NHGRI NIH HHS
• R21 DK084554 NIDDK NIH HHS
• UL1 TR000124 NCATS NIH HHS
• P01DK046763 NIDDK NIH HHS
• DK46763 NIDDK NIH HHS
• R21 HG005964 NHGRI NIH HHS
• R01 AI078885 NIAID NIH HHS
• P01 DK046763 NIDDK NIH HHS
• AI078885 NIAID NIH HHS
• DK062413 NIDDK NIH HHS
• DK084554 NIDDK NIH HHS

Innate immune recognition of bacteria is the first requirement for mounting an effective immune response able to control infection. Over the previous decade, the general paradigm was that extracellular bacteria were only sensed by cell surface-expressed Toll-like receptors (TLRs), whereas cytoplasmic sensors, including members of the Nod-like receptor (NLR) family, were specific to pathogens capable of breaching the host cell membrane. It has become apparent, however, that intracellular innate immune molecules, such as the NLRs, play key roles in the sensing of not only intracellular, but also extracellular bacterial pathogens or their components. In this review, we will discuss the various mechanisms used by bacteria to activate NLR signaling in host cells. These mechanisms include bacterial secretion systems, pore-forming toxins, and outer membrane vesicles. We will then focus on the influence of NLR activation on the development of adaptive immune responses in different cell types.

• NLRs
• OMVs
• adaptive immunity
• extracellular bacteria
• innate immunity

Ulcerative colitis (UC) is an inflammation-associated disease of the colon and rectum. The onset and progress of the disease are directly influenced by the nature of the intestinal microflora, the intestinal barrier function, and the immunological responses of the host. The epithelial invasion of pathogenic bacteria due to excess contact and/or barrier dysfunction is related to inflammation mediated by intestinal immune responses. Although the etiology of UC is not clearly understood, recent studies have shown a rising incidence of UC worldwide, and this phenomenon is more prominent in Asian countries and in Asian immigrants in Western countries. The increased prevalence of UC also contributes to an increased risk of developing colorectal cancer. Environmental factors, including changes in dietary habits, have been suggested as major risk factors of UC. A systematic review showed a negative association between UC risk and vegetable intake, whereas total fat, omega-6 fatty acids and meat intake were positively associated with an increased risk of UC. Individual dietary factors and energy balance have been suggested as having important roles in inducing changes in the microbial population and intestinal barrier integrity and in regulating inflammatory immune responses, directly or indirectly. Excess energy intake is now known to increase pathogenic microbial populations. Likewise, the application of appropriate probiotics may reverse the pathogenic progression of the disease. In the meantime, dietary anti-inflammatory compounds, including omega-3 fatty acids and other phytochemicals, may directly suppress inflammatory responses in the course of UC development. In this review, the increased prevalence of UC and its management are interpreted from the standpoint of nutritional modulation to regulate the intestinal microflora population, intestinal epithelium permeability, and inflammatory responses.

• Ulcerative colitis
• Intestinal microflora
• Immunity
• Inflammation
• Clinical
• Obesity
• Probiotics
• Omega-3 fatty acids
• Antioxidants

• Animals
• Anti-Inflammatory Agents/therapeutic use
• Antioxidants/therapeutic use
• Colitis, Ulcerative/epidemiology
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/microbiology
• Colitis, Ulcerative/physiopathology
• Colitis, Ulcerative/therapy
• Diet/adverse effects
• Energy Intake
• Feeding Behavior
• Humans
• Intestines/immunology
• Intestines/microbiology
• Intestines/physiopathology
• Nutrition Assessment
• Nutritional Status
• Permeability
• Prevalence
• Probiotics
• Prognosis
• Risk Factors
• Risk Reduction Behavior