Submucosal glands produce most of nasal mucous secretion which play an important role in airflow hydration, mucociliary transport, innate immunity and antimicrobial defense. However, excessive mucus secretion is related with pathophysiologic characteristics in several chronic inflammatory diseases such as chronic rhinosinusitis and allergic rhinitis. This review details the anatomy, physiology of submucosal gland in nose and summarized pathophysiologic relationship between the submucosal gland and nasal diseases.
Immunity, Innate ; Mucociliary Clearance ; Mucus ; Nose Diseases ; Nose* ; Physiology ; Rhinitis

Toll like receptor (TLR) can specifically recgnize pathogen-associated molecular patterns (PAMPs) and is considered as an important link between innate and adaptive immunity. It has been shown that TLR plays an important role in the pathogenesis and pathophysiology of a variety of skin diseases. Moreover, TLR agonists have exhibited promising therapeutic effects on the disease models and are expected to be novel vaccine adjuvants. Investigations of the underlying mechanism will give new insights into these diseases. This review will discuss the relationship between TLR and pathogenesis and management of some cutaneous diseases.
Adaptive Immunity ; Immunity, Innate ; Signal Transduction ; Skin Diseases ; immunology ; metabolism ; Toll-Like Receptors ; immunology ; metabolism ; physiology

OBJECTIVETo review the senescent remodeling of the immune system with aging and its relevance to the increased susceptibility of the elderly to infectious diseases, along with an outlook on emerging immunological biomarkers.

DATA SOURCESThe data selected were from PubMed with relevant published articles in English or French from 1995 to the present. Searches were made using the terms "immunosenescence" and "aging" paired with the following: "innate immunity", "T-cell", "B-cell", "adaptive immunity" and "biomarkers". Articles were reviewed for additional citations and some information was gathered from web searches.

STUDY SELECTIONArticles on aging of both the innate and adaptive immunity were reviewed, with special attention to the remodeling effect on the ability of the immune system to fight infectious diseases. Articles related to biomarkers of immunosenescence were selected with the goal of identifying immunological biomarkers predisposing the elderly to infections.

RESULTSInnate immunity is generally thought to be relatively well preserved or enhanced during aging compared with adaptive immunity which manifests more profound alterations. However, evidence, particularly in the last decade, reveals that both limbs of the immune system undergo profound remodeling with aging. Reported data on adaptive immunity is consistent and changes are well established but conflicting results about innate immunity were reported between in vivo and in vitro studies, as well as between murine and human studies. Epidemiological data suggests increased predisposition of the elderly to infections, but no compelling scientific evidence has directly linked senescent immune remodeling to this increased susceptibility. Recently, growing interest in identifying immunological biomarkers and defining "immune risk phenotypes/profiles" (IRP) has been expressed. Identification of biomarkers is in its early days and few potential biomarkers have been identified, with the Swedish having defined one IRP based on the adaptive immune response.

CONCLUSIONSAging does not necessarily lead to an unavoidable decline in immune functions. Instead, a complex remodeling occurs. Despite the lack of compelling scientific evidence, senescent immune remodeling surely is a significant contributing factor to the increased risk and severity of infections in the elderly. Although, no immunological biomarker has been formally linked to the increased risk of infections in the elderly, biomarkers remain a promising tool to predict the likelihood of healthy aging, the level of immune competence, and mortality risk in the elderly. Hence, more research is required to define healthy aging and identify immunological biomarkers.

Adaptive Immunity ; immunology ; Aging ; immunology ; physiology ; Animals ; Humans ; Immune System ; immunology ; Immunity, Innate ; immunology ; Infection ; immunology

Autophagy is a housekeeping process that maintains cellular homeostasis through recycling of nutrients and degradation of damaged or aged cytoplasmic constituents. Over the past several years, accumulating evidence has suggested that autophagy can function as an intracellular innate defense pathway in response to infection with a variety of bacteria and viruses. Autophagy plays a role as a specialized immunologic effector and regulates innate immunity to exert antimicrobial defense mechanisms. Numerous bacterial pathogens have developed the ability to invade host cells or to subvert host autophagy to establish a persistent infection. In this review, we have summarized the recent advances in our understanding of the interaction between antibacterial autophagy (xenophagy) and different bacterial pathogens.
Animals ; Autophagy/*physiology ; Bacterial Infections/*immunology/metabolism ; Humans ; Immunity, Innate/physiology ; Reactive Oxygen Species/metabolism

The picornavirus family comprises many small viruses, several of which are important pathogens of humans and livestock. The 3C protease (3Cpro) of different species and genera of picornavirus contains the classic G-X-C-G motif and Cys-His-Asp/Glu catalytic triad. 3Cpro conducts maturation cleavage in the regions of VP2-VP3 and VP3-VP1 in P1, 2A-2B and 2B-2C in P2 and the whole P3. Picornavirus 3Cpro has been shown to have significant substrate preference in Q-G/S/A/V/H/R and E-S/G/R/M as well as species and genera specificity through analyses of the maturation cleavage of picornavirus polyproteins. Innate immune adaptors such as TRIF, MAVS, IRF3, IRF7 and NEMO have various potential cleavage sites in picornavirus 3Cpro (TRIF and NEMO show considerable diversity in their cleavage sites). Useful information will be provided for the development of broad-spectrum antiviral agents as well as evasion mechanisms of the innate immune system against picornavirus 3Cpro through continued research of picornavirus 3Cpro.
Cysteine Endopeptidases ; physiology ; Immunity, Innate ; Picornaviridae ; enzymology ; immunology ; Viral Proteins ; physiology ; Virus Replication

OBJECTIVETo identified the resistance of Coix to Ustilago coicis and screen the high disease-resistance Coix germplasm.

METHODField and laboratory biochemical methods were used for the resistance identification. Ninteen germplasms collected from 7 provinces in southern of China such as Yunnan, Zhejiang, Fujian etc. were inoculated with chlamydospore of U. coicis, respectively. The incidence of a disease in field was investigated and the level of resistance was evaluated. The PAL activity dynamic changes in different level resistant germplasms were further determined.

RESULTThe result of field test showed 1 germplasm was immune, 1 germplasm was high resistance which incidence rate was under 20%, 6 germplasms were moderate resistance with the average incidence rates ranged within 20% - 40%, 11 of 19 germplasms that average incidence rates above 40% were identified as sensitive resistance. The value of PLA activity peak of resistant germplasm in seedling was significant higher and appeared earlier than that of the sensitive ones after inoculating.

CONCLUSIONMost collected C. lacryma-jobi germplasms are sensitive to smut in our investigation; the PAL activity may play important role in Coix germplasm for resistance to smut and the biochemical method may be as an aiding method to resistance identification of Coix germplasm.

China ; Coix ; immunology ; microbiology ; Immunity, Innate ; Plant Diseases ; immunology ; microbiology ; Ustilago ; physiology

Dendritic cells (DCs), the most potent antigen-presenting cells, recognize pathogen by Toll-like receptors (TLRs) and serve as the bridge between the innate and the adaptive immune responses. TLRs-mediated signal transduction plays a crucial role in the functional maturation of DCs. This review summarizes the research progress on the expression and function of TLRs in DCs.
Dendritic Cells ; immunology ; metabolism ; Humans ; Immunity, Innate ; Signal Transduction ; Toll-Like Receptors ; metabolism ; physiology

Innate lymphoid cells (ILCs) are a newly classified family of immune cells of the lymphoid lineage. While they could be found in both lymphoid organs and non-lymphoid tissues, ILCs are preferentially enriched in barrier tissues such as the skin, intestine, and lung where they could play important roles in maintenance of tissue integrity and function and protection against assaults of foreign agents. On the other hand, dysregulated activation of ILCs could contribute to tissue inflammatory diseases. In spite of recent progress towards understanding roles of ILCs in the health and disease, mechanisms regulating specific establishment, activation, and function of ILCs in barrier tissues are still poorly understood. We herein review the up-to-date understanding of tissue-specific relevance of ILCs. Particularly we will focus on resident ILCs of the skin, the outmost barrier tissue critical in protection against various foreign hazardous agents and maintenance of thermal and water balance. In addition, we will discuss remaining outstanding questions yet to be addressed.
Animals ; Humans ; Immunity, Innate ; physiology ; Inflammation ; immunology ; Lymphocytes ; immunology ; Skin ; immunology

Pattern recognition receptors (PRRs) in innate immune cells play a pivotal role in the first line of host defense system. PRRs recognize pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) to initiate and regulate innate and adaptive immune responses. PRRs include Toll-like receptors (TLRs), RIG-I-like receptors (RLRs) and NOD-like receptors (NLRs), which have their own features in ligand recognition and cellular location. Activated PRRs deliver signals to adaptor molecules (MyD88, TRIF, MAL/TIRAP, TRAM, IPS-1) which act as important messengers to activate downstream kinases (IKK complex, MAPKs, TBK1, RIP-1) and transcription factors (NF-kappaB, AP-1, IRF3), which produce effecter molecules including cytokines, chemokines, inflammatory enzymes, and type I interferones. Since excessive PRR activation is closely linked to the development of chronic inflammatory diseases, the role of intrinsic and extrinsic regulators in the prevention of over- or unnecessary activation of PRRs has been widely studied. Intracellular regulators include MyD88s, SOCS1, TOLLIP, A20, and CYLD. Extrinsic regulators have also been identified with their molecular targets in PRR signaling pathways. TLR dimerization has been suggested as an inhibitory target for small molecules such as curcumin, cinnamaldehyde, and sulforaphane. TBK1 kinase can be a target for certain flavonoids such as EGCG, luteolin, quercetin, chrysin, and eriodictyol to regulate TRIF-dependent TLR pathways. This review focuses on the features of PRR signaling pathways and the therapeutic targets of intrinsic and extrinsic regulators in order to provide beneficial strategies for controlling the activity of PRRs and the related inflammatory diseases and immune disorders.
Adaptive Immunity ; Gene Expression Regulation ; Humans ; *Immunity, Innate ; *Models, Immunological ; Receptors, Pattern Recognition/genetics/metabolism/*physiology ; Signal Transduction ; Toll-Like Receptors/genetics/metabolism/physiology ; Transcription Factors/physiology

With growing accounts of inflammatory diseases such as sepsis, greater understanding the immune system and the mechanisms of cellular immunity have become primary objectives in immunology studies. High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that is implicated in various aspects of the innate immune system as a damage-associated molecular pattern molecule and a late mediator of inflammation, as well as in principal cellular processes, such as autophagy and apoptosis. HMGB1 functions in the nucleus as a DNA chaperone; however, it exhibits cytokine-like activity when secreted by injurious or infectious stimuli. Extracellular HMGB1 acts through specific receptors to promote activation of the NF-kappaB signaling pathway, leading to production of cytokines and chemokines. These findings further implicate HMGB1 in lethal inflammatory diseases as a crucial regulator of inflammatory, injurious, and infectious responses. In this paper, we summarize the role of HMGB1 in inflammatory and non-inflammatory states and assess potential therapeutic approaches targeting HMGB1 in inflammatory diseases.
Amino Acid Sequence ; HMGB1 Protein/chemistry/metabolism/*physiology ; Humans ; Immunity, Innate/*physiology ; *Models, Immunological ; Molecular Sequence Data ; Protein Structure, Tertiary ; Signal Transduction