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INFLAMATORY FACTORS OF NASAL POLYP OLEH:

DINA AULIA, S.KED


INTRODUCTION

Nasal
Most common mass lession of the nose even
4000 years ago in Egypt
Multifactorial caused pathogenic disorders,
polyp allergy, infection, cystic fibrosis, asthma, and
aspirin intolerance

0,2 to 4,3% worldwide


ratio 2-3:1; male: female
Prevalence

Presents between the ages of 30-60 yo
Dominantly of eosinophil and neutrophil
inflamations.
Nasal polyps are abnormal lesions that originate from any
portion of the nasal mucosa or paranasal sinuses.

Multiple polyps can occur in children with chronic sinusitis,


allergic rhinitis, cystic fibrosis (CF), or allergic fungal
sinusitis (AFS).

polyp could be an antral-choanal polyp, a benign massive


polyp, or any benign or malignant tumor.
DEFINITION
linked to abnormal
chronic lesions
inflammation

benign
semitransparent
nasal lesions
THE FOLLOWING CONDITIONS ARE ASSOCIATED WITH MULTIPLE BENIGN POLYPS:
Bronchial asthma - In 20-50% of patients with polyps

CF - Polyps in 6-44% of patients with CF [1]

Allergic rhinitis

AFS - Polyps in 85% of patients with AFS

Chronic rhinosinusitis

Primary ciliary dyskinesia

Aspirin intolerance - In 8-26% of patients with polyps

Alcohol intolerance - In 50% of patients with nasal polyps

Churg-Strauss syndrome - Nasal polyps in 50% of patients with Churg-Strauss syndrome

Young syndrome (ie, chronic sinusitis, nasal polyposis, azoospermia)

Nonallergic rhinitis with eosinophilia syndrome (NARES) - Nasal polyps in 20% of patients with
NARES
In Bernstein's theory, inflammatory
polyps are an exvagination of changes first occur in the lateral
Most studies suggest the normal nasal or sinus mucosa nasal wall or sinus mucosa as the
nonallergic disease that fills with edematous stroma result of viral-bacterial host
interactions or secondary to
turbulent airflow

inflammatory process from


epithelial cells, vascular
Ulceration or prolapse of the endothelial cells, and fibroblasts
submucosa can occur, with affects the bioelectric integrity of
reepithelialization and new gland the sodium channels at the luminal
formation. surface of the respiratory
epithelial cell in that section of
the nasal mucosa
OTHER THEORIES

increased vascular stroma result in marked


permeability and impaired nvolve vasomotor
vascular regulation cause edema worsened by imbalance or epithelial
detoxification of mast-cell venous drainage rupture
products (eg, histamine) obstruction
NASAL POLYP
PATHOGENESIS OF NASAL POLYP
POTENTIAL ROLE FOR MICROBIAL
COLONIZATION

fungi Staphylococcus
(alternaria) aureus
inflammatory Elevated levels of
disease activate large superantigen-binding T cells
numbers of T cells
mechanism in NP have been identified
by flow cytometry
epithelial bind a large
damage and fraction of T cell
activation of receptors via the
adaptive immune
responses V region
have superantigen-specific
IgE in their NP
peptide
processing and
MHCII
DEFECTS IN AIRWAY EPITHELIAL CELL
INNATE IMMUNE FUNCTIONS

type 2 cytokines, such as influx of foreign antigens


The epithelial layer of IL-4 and IL-13 into the submucosa where
the airways provides a proinflammatory they may trigger or
first line of defence cytokines, such as exacerbate an
oncostatin M (OSM) inflammatory response
CONT...

epithelial cells have epithelial cells express elevated expression of


inducible innate immune pattern recognition TLR2, TLR4, TLR7 and/or
functions receptors (PRRs), such as TLR9
tolllike receptors (TLRs)
ALTERED EXPRESSION OF CYTOKINES
AND CHEMOKINES

Chemokines important for the attraction of eosinophils, neutrophils, macrophages,


dendritic cells, T cells and B cells, have all been reported to be elevated

romote type 2 inflammation Eotaxin 1 (CCL11), along with eotaxins 2 and 3


(CCL24 and CCL26,

respectively), is among the main CCR3-activating chemokines responsible for


recruitment of eosinophils

ion of CCL11 by NP-derived fibroblasts, or airway epithelial cells, has been shown
to be increased by the combination of IL-4, or IL-13, and TNF
CONT...
Cytokines that play an important role in the skewing of
adaptive immune responses

traditional type 2 cytokines (IL-4, IL-5 and IL-13)

This cytokine is known to play an important role in the


activation and survival of B cells in secondary lymphoid
organs and could play an important role in the accumulation
of activated B cell subsets and antibodies in NP
TYPE 2 INFLAMMATION IN THE MEDIATION
INNATE IMMUNE EFFECTOR CELLS
Mast cells are important
This includes monocytes, sentinels of the immune
cytokines and chemokines are macrophages, dendritic cells, system, and they are ideally
important for initiating and neutrophils, mast cells, located to detect and rapidly
perpetuating tissue eosinophils, basophils and respond to pathogens at
inflammatory responses ILC2s mucosal surfaces elevated
mast cells

Innate lymphoid cells (ILCs)


basophils also play an It is well documented that CD4+ T cells IL-5 and IL-
important role in type 2 eosinophils are highly 13 epitelial derivate
immune responses elevated in NP tissues as well. cytokine IL-25, IL-33, and
TSLP
EXPANSION OF T CELLS, B CELLS AND PLASMA CELLS OCCURS WITH THE HELP OF
LOCAL DENDRITIC CELLS, RESULTING IN THE PRODUCTION OF CYTOKINES AND
IMMUNOGLOBULINS AT HIGH LEVELS IN THE TISSUE
ADAPTIVE IMMUNITY

Cytokine IFN-
, IL-17+ and IL-
activation of B 10+
cell responses
Th2 cells rising and can produce
pro-inflammatory
cytokines within
the tissue