Autophagy is a crucial biological process of eukaryotes, which is involved in cell growth, survival and energy metabolism, while the premise of the autophagy function is activated autophagic flux. It has been confirmed that impaired autophagic flux promotes pathogenesis of many chronic inflammatory diseases, especially cancer, neurodegenerative disease and tissue fibrosis, therefore the analysis of autophagic flux state is important for revealing autophagy function and the mechanism of autophagy related diseases. Given that autophagy is a dynamic process with multiple steps, it is very hard to observe the real state of autophagic flux. Summarized here is the novel concept and current approach to detect autophagic flux. This knowledge is crucial for the researching of the biological function of autophagy, and may provide some strategies for developing autophagy-related drug.
Autophagy ; Fibrosis ; Humans ; Inflammation ; pathology ; Neoplasms ; pathology ; Neurodegenerative Diseases ; pathology

Cartilage Diseases ; Ear Auricle ; pathology ; Humans ; Inflammation

Bronchial asthma is a heterogeneous chronic inflammatory disease involving multiple immune cells and structural cells.It is characterized by airflow limitation,airway hyperresponsiveness,and airway remodeling,with complex pathogenesis.In recent years,the research on exosomes has developed rapidly.Exosomes are small vesicles secreted by a variety of cells and are naturally found in various biological fluids,with stability and biocompatibility.Exosomes from different cells are involved in pathophysiological processes such as airway inflammation,remodeling,and hyperresponsiveness through specific mechanisms and play a regulatory role in multiple links in bronchial asthma.This review focuses on the role of exosomes from different cells in the pathogenesis of bronchial asthma.
Humans ; Exosomes/pathology* ; Asthma ; Lung/pathology* ; Inflammation ; Chronic Disease

Cellular immune responses as well as generalized and periarticular bone loss are the key pathogenic features of rheumatoid arthritis (RA). Under the pathological conditions of RA, dysregulated inflammation and immune processes tightly interact with skeletal system, resulting in pathological bone damage via inhibition of bone formation or induction of bone resorption. Single-cell omics technologies are revolutionary tools in the field of modern biological research.They enable the display of the state and function of cells in various environments from a single-cell resolution, thus making it conducive to identify the dysregulated molecular mechanisms of bone destruction in RA as well as the discovery of potential therapeutic targets and biomarkers. Here, we summarize the latest findings of single-cell omics technologies in osteoimmunology research in RA. These results suggest that single-cell omics have made significant contributions to transcriptomics and dynamics of specific cells involved in bone remodeling, providing a new direction for our understanding of cellular heterogeneity in the study of osteoimmunology in RA.
Humans ; Osteoclasts/physiology* ; Arthritis, Rheumatoid/pathology* ; Inflammation/pathology* ; Bone and Bones/pathology* ; Bone Resorption/pathology*

The pattern of metabolism changes obviously after severe burn trauma, and it is characterized by an immensely increase in energy consumption, persistent strengthening in catabolism, and impediment of utilization of nutrient substrate. It will lead to autophagy, continuous consumption, and progressive emaciation, etc. If these pathological phenomena can not be effectively corrected, the prognosis of patients with serious burn will be poor, with complications of organ damage, immune dysfunction, and delayed wound healing, etc. Hypermetabolism after burn has become one of the leading causes of multiple organ dysfunction and even death. After many years' research, we have a certain understanding of burn hypermetabolism, but it is still difficult to clearly explain the mechanism up to now. Moreover, the measures of regulating hypermetabolism are still not perfect, hampering the advance of treatment of serious burn trauma. The purpose of the article is to analyze and discuss the essential mechanism of hypermetabolism after burn, basing on the new literature and a series of our experimental and clinical studies. Meanwhile the regulation strategy concerning burn hypermetabolism is proposed. It focuses on regulation of endocrine and inflammatory mediators, as well as maintenance of gastrointestinal structure and function.
Burns ; metabolism ; pathology ; therapy ; Endocrine System ; Gastrointestinal Tract ; Humans ; Inflammation ; Inflammation Mediators

OBJECTIVETo investigate the pathologic features of histologic chorioamnionitis (HCA) and its impact on newborns.

METHODSFrom Jun.2012 to Dec.2014, 5 810 placentas delivered in our hospital were collected. There were 898 HCA cases and positive rate was 18.3%.Cases with complete clinical data were collected, including 308 cases of infected newbon infants (case group), and 120 cases of non-infected infants(control group). The correlation between pathologic results and neonatal outcome was analyzed.

RESULTSThirty nine cases were premature delivery (39/428, 9.1%). Twenty one cases were small for gestational age (21/428, 4.9%). One hundred and eleven cases were delivered by caesarean section (111/428, 25.9%). Three hundred and eight cases of neonatal infection included 104 cases of hematosepsis, 16 cases of purulent meningitis, 78 cases of infectious pneumonia, 34 cases of infective enteritis, 18 cases of urinary tract infection and 58 cases of skin infection.Placental pathological examination found out 40 cases showed mild HCA (18 cases of neonatal infection, and 22 non-neonatal infection cases), 104 cases showed moderate HCA (88 cases of neonatal infection, and 16 non-neonatal infection cases), and 183 cases showed severe HCA (172 cases of neonatal infection and 11 non-neonatal infection cases). Moderate to severe HCA were easily found in premature infants, with higher positive rate of both late pregnancy group B streptococcus (P<0.05) and afterbirth blood culture (P<0.05). Significantly higher serum C reaction protein (P<0.05) and white-cell count(P<0.05) were also found within moderate to severe HCA patients. Moderate to severe HCA, funisitis and syncytial nodular hyperplasia were associated with neonatal infections (P<0.05), while infarction, intervillous thrombosis and villi thrombus were not observed in the inflammation group (P>0.05).

CONCLUSIONSHCA is often of few clinical symptoms and easily misdiagnosed by placental pathological assessment only. HCA is found associated with intrauterine infection and neonatal infection. Pathological assessment of placenta is valuable in diagnosis and treatment of intrauterine infection.

Chorioamnionitis ; pathology ; Female ; Humans ; Infant, Newborn ; Inflammation ; pathology ; Leukocyte Count ; Placenta ; pathology ; Pregnancy

Asthma, Occupational ; etiology ; pathology ; Humans ; Inflammation ; pathology ; Neutrophil Infiltration ; Neutrophils ; pathology

Chronic Disease ; Humans ; Inflammation ; diagnosis ; pathology ; Nasal Mucosa ; pathology ; Paranasal Sinuses ; pathology

Multiple sclerosis (MS) is regarded as a chronic inflammatory disease that leads to demyelination and eventually to neurodegeneration. Activation of innate immune cells and other inflammatory cells in the brain and spinal cord of people with MS has been well described. However, with the innovation of technology in glial cell research, we have a deep understanding of the mechanisms of glial cells connecting inflammation and neurodegeneration in MS. In this review, we focus on the role of glial cells, including microglia, astrocytes, and oligodendrocytes, in the pathogenesis of MS. We mainly focus on the connection between glial cells and immune cells in the process of axonal damage and demyelinating neuron loss.
Humans ; Multiple Sclerosis ; Neuroglia ; Inflammation/pathology* ; Brain/pathology* ; Spinal Cord/pathology*

OBJECTIVE: To summarize the research progress on the role of macrophage-mediated osteoimmune in osteonecrosis of the femoral head (ONFH) and its mechanisms. METHODS: Recent studies on the role and mechanism of macrophage-mediated osteoimmune in ONFH at home and abroad were extensively reviewed. The classification and function of macrophages were summarized, the osteoimmune regulation of macrophages on chronic inflammation in ONFH was summarized, and the pathophysiological mechanism of osteonecrosis was expounded from the perspective of osteoimmune, which provided new ideas for the treatment of ONFH. RESULTS: Macrophages are important immune cells involved in inflammatory response, which can differentiate into classically activated type (M1) and alternatively activated type (M2), and play specific functions to participate in and regulate the physiological and pathological processes of the body. Studies have shown that bone immune imbalance mediated by macrophages can cause local chronic inflammation and lead to the occurrence and development of ONFH. Therefore, regulating macrophage polarization is a potential ONFH treatment strategy. In chronic inflammatory microenvironment, inhibiting macrophage polarization to M1 can promote local inflammatory dissipation and effectively delay the progression of ONFH; regulating macrophage polarization to M2 can build a local osteoimmune microenvironment conducive to bone repair, which is helpful to necrotic tissue regeneration and repair to a certain extent. CONCLUSION At present, it has been confirmed that macrophage-mediated chronic inflammatory immune microenvironment is an important mechanism for the occurrence and development of ONFH. It is necessary to study the subtypes of immune cells in ONFH, the interaction between immune cells and macrophages, and the interaction between various immune cells and macrophages, which is beneficial to the development of potential therapeutic methods for ONFH.
Humans ; Femur Head/pathology* ; Osteonecrosis/therapy* ; Macrophages/pathology* ; Inflammation ; Femur Head Necrosis/pathology*