Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice.
Study subjects
Pure PM2.5 BALB/c mouse
BALB/c mice. The abstract describes no separate allergen sensitization or challenge step; PM2.5 itself was administered. Age and body weight are not given in the abstract.
Treated PM2.5 BALB/c mouse
BALB/c mice. The abstract describes no separate allergen sensitization or challenge step; acid- and heat-treated PM2.5 was administered. Age and body weight are not given in the abstract.
Lung function assays
Airway hyperresponsiveness - pure PM2.5
AHR in BALB/c mice administered untreated (pure) PM2.5 collected by the cyclone system. This is the intact-particle arm: protein and trace elements still bound. The abstract reports that this PM2.5 induced allergic airway inflammation in mice but gives no AHR value.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | AHR - pure PM2.5 group LF:ogino-ahr-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5 collected by of the cyclone system induced allergic airway inflammation in mice.
The paper's own conclusion that the intact, cyclone-collected PM2.5 induced allergic airway inflammation in the mouse. Airway hyperresponsiveness is one of the endpoints by which that inflammation was compared between groups, so this sentence establishes the pure-PM2.5 arm this assay records.
Airway hyperresponsiveness - acid/heat-treated PM2.5
AHR in BALB/c mice administered PM2.5 whose bound protein had been hydrolyzed and whose trace elements had been removed by high-temperature strong-acid treatment. AHR was attenuated relative to pure PM2.5, so PM2.5-bound protein and acid-soluble metals are required for the airway hyperresponsiveness. The abstract reports attenuation without a value or p-value.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | AHR - treated PM2.5 group LF:ogino-ahr-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
The treatment of PM2.5 with a strong acid at a high temperature attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation.
States directly that the strong-acid, high-temperature treatment — the treatment the abstract elsewhere says hydrolyzes PM2.5-bound protein and removes trace elements — attenuated AHR. That attenuation is what this treated-PM2.5 output record captures.
BALF sputum assays
BALF inflammatory cell differential - pure PM2.5
BALF eosinophil and neutrophil percentages in mice given untreated PM2.5. This is the reference arm against which the acid/heat-treated particle is compared. The abstract gives no percentages for either arm.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | BALF cell percentages - pure PM2.5 group BALF:ogino-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
Allergic airway inflammation was compared between the three groups (saline, pure PM2.5 and treated PM2.5) by evaluating airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF) cells, serum IgE, the mRNA of various cytokine (IL-4, IL-5, IL-13, eotaxin-1 and CXCL3), mucus protein mRNA (MUC5ac and MUC5b) and the filtration of inflammatory cells in the lung.
Establishes that BALF cells were measured in a pure PM2.5 group alongside a saline group and a treated PM2.5 group, which is exactly the group structure and endpoint this assay record represents.
BALF inflammatory cell differential - acid/heat-treated PM2.5
BALF eosinophil and neutrophil percentages in mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Eosinophil percentage was attenuated, while neutrophil percentage was increased: removing the protein and metal fraction removes the eosinophilic (allergic) cell response but leaves a neutrophilic response driven by the residual particle core.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | BALF cell percentages - treated PM2.5 group BALF:ogino-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
The treatment of PM2.5 with a strong acid at a high temperature attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation.
Supports the eosinophil half of this output record: the acid/heat treatment that removes PM2.5-bound protein and trace elements attenuated the BALF eosinophil percentage.
the percentage of neutrophils in BALF
Supports the neutrophil half of this output record. In the abstract this phrase heads the list introduced by "On the contrary," and closed by "was increased", i.e. the BALF neutrophil percentage rose in the treated-PM2.5 group while the eosinophil percentage fell. Quoted as a fragment because the full sentence contains a non-ASCII character (MIP2a is written with a Greek alpha) that the committed cache renders in a form a whole-sentence quote cannot be guaranteed to reproduce.
Gene expression assays
IL-13 mRNA in lung - pure PM2.5
IL-13 mRNA in lung of mice given untreated PM2.5. Reference arm for the IL-13 comparison. IL-13 is named in the abstract's list of cytokine mRNAs evaluated across the three groups; no value is reported.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | IL-13 mRNA - pure PM2.5 group GE:ogino-il13-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
the mRNA of various cytokine (IL-4, IL-5, IL-13, eotaxin-1 and CXCL3)
Establishes that IL-13 mRNA was one of the cytokine transcripts measured and compared across the saline, pure PM2.5 and treated PM2.5 groups, which is what this pure-PM2.5 reference record holds.
IL-13 mRNA in lung - acid/heat-treated PM2.5
IL-13 mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Attenuated relative to pure PM2.5, so the Th2 cytokine response depends on the PM2.5-bound protein and acid-soluble metal fraction rather than on the particle core.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | IL-13 mRNA - treated PM2.5 group GE:ogino-il13-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation
The abstract's result sentence names IL-13 mRNA among the endpoints attenuated by the strong-acid, high-temperature treatment. That is the decrease this treated-PM2.5 output record captures.
CXCL3 mRNA in lung - pure PM2.5
CXCL3 mRNA in lung of mice given untreated PM2.5. Reference arm for the CXCL3 comparison. No value is reported in the abstract.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | CXCL3 mRNA - pure PM2.5 group GE:ogino-cxcl3-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
the mRNA of various cytokine (IL-4, IL-5, IL-13, eotaxin-1 and CXCL3)
Establishes that CXCL3 mRNA was among the transcripts measured and compared across the saline, pure PM2.5 and treated PM2.5 groups, which is what this pure-PM2.5 reference record holds.
CXCL3 mRNA in lung - acid/heat-treated PM2.5
CXCL3 mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Attenuated relative to pure PM2.5.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | CXCL3 mRNA - treated PM2.5 group GE:ogino-cxcl3-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation
The abstract's result sentence names CXCL3 mRNA among the endpoints attenuated by the strong-acid, high-temperature treatment that removes PM2.5-bound protein and trace elements.
MIP2a mRNA in lung - pure PM2.5
MIP2a (CXCL2) mRNA in lung of mice given untreated PM2.5. Reference arm for the MIP2a comparison. The abstract reports MIP2a only in the treated-versus-pure contrast, with no value for either arm.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | MIP2a mRNA - pure PM2.5 group GE:ogino-mip2a-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice.
Establishes the pure-versus-treated particle contrast that this reference record is the pure arm of: the acid/heat treatment is what hydrolyzes the bound protein and removes the trace elements, so the untreated particle is the comparator against which the MIP2a increase is read.
MIP2a mRNA in lung - acid/heat-treated PM2.5
MIP2a (CXCL2, a neutrophil chemoattractant) mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Increased relative to pure PM2.5, tracking the rise in BALF neutrophils: the residual, carbon-enriched particle core drives a neutrophilic rather than eosinophilic chemokine program.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | MIP2a mRNA - treated PM2.5 group GE:ogino-mip2a-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
On the contrary, the percentage of neutrophils in BALF, mRNA expression of MIP2
The abstract's contrary-direction sentence lists MIP2a mRNA among the endpoints that rose in the treated-PM2.5 group (the sentence closes "... was increased"). Quoted as a fragment stopping before the Greek alpha in MIP2a so the span is exact ASCII text present verbatim in the committed cache entry.
TLR4 mRNA in lung - pure PM2.5
TLR4 mRNA in lung of mice given untreated PM2.5. Reference arm for the TLR4 comparison. No value is reported in the abstract.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | TLR4 mRNA - pure PM2.5 group GE:ogino-tlr4-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice.
Establishes the untreated-particle comparator arm that this record holds, against which the abstract's reported TLR4 mRNA increase in the treated group is read.
TLR4 mRNA in lung - acid/heat-treated PM2.5
TLR4 mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Increased relative to pure PM2.5 — innate pattern-recognition signalling rises as the allergic arm falls, consistent with the shift from an eosinophilic to a neutrophilic response once the protein and metal fraction is gone.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | TLR4 mRNA - treated PM2.5 group GE:ogino-tlr4-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
EGFR, Nrf2, and TLR4 and 4-OH-2-nonenal levels in the lung was increased.
Names TLR4 mRNA among the endpoints the abstract reports as increased in the acid/heat-treated PM2.5 group. Quoted from the point after the Greek alpha in MIP2a so the span is exact ASCII text present verbatim in the committed cache entry.
EGFR mRNA in lung - pure PM2.5
EGFR mRNA in lung of mice given untreated PM2.5. Reference arm for the EGFR comparison. No value is reported in the abstract.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | EGFR mRNA - pure PM2.5 group GE:ogino-egfr-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice.
Establishes the untreated-particle comparator arm that this record holds, against which the abstract's reported EGFR mRNA increase in the treated group is read.
EGFR mRNA in lung - acid/heat-treated PM2.5
EGFR mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Increased relative to pure PM2.5. Note the abstract reports EGFR at the mRNA level only; it makes no claim about receptor phosphorylation or downstream signalling.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | EGFR mRNA - treated PM2.5 group GE:ogino-egfr-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
EGFR, Nrf2, and TLR4 and 4-OH-2-nonenal levels in the lung was increased.
Names EGFR mRNA among the endpoints the abstract reports as increased in the acid/heat-treated PM2.5 group, which is the increase this output record captures.
Nrf2 mRNA in lung - pure PM2.5
Nrf2 mRNA in lung of mice given untreated PM2.5. Reference arm for the Nrf2 comparison. No value is reported in the abstract.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | Nrf2 mRNA - pure PM2.5 group GE:ogino-nrf2-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice.
Establishes the untreated-particle comparator arm that this record holds, against which the abstract's reported Nrf2 mRNA increase in the treated group is read.
Nrf2 mRNA in lung - acid/heat-treated PM2.5
Nrf2 mRNA in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Increased relative to pure PM2.5. Nrf2 is the antioxidant-response transcription factor; its induction alongside the rise in 4-OH-2-nonenal indicates the residual particle core imposes more oxidative stress than the intact particle did.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | Nrf2 mRNA - treated PM2.5 group GE:ogino-nrf2-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
EGFR, Nrf2, and TLR4 and 4-OH-2-nonenal levels in the lung was increased.
Names Nrf2 mRNA among the endpoints the abstract reports as increased in the acid/heat-treated PM2.5 group, in the same clause as the 4-OH-2-nonenal rise.
Oxidative stress assays
Lung 4-OH-2-nonenal - pure PM2.5
4-OH-2-nonenal (4-hydroxy-2-nonenal), a lipid peroxidation end-product, measured in lung of mice given untreated PM2.5. Reference arm for the 4-HNE comparison. No value is reported in the abstract.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Pure (untreated) PM2.5 administration EXPOSURE:ogino-pure-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | Lung 4-OH-2-nonenal - pure PM2.5 group OX:ogino-4hne-pure-pm25-output · under EXPOSURE:ogino-pure-pm25 |
Evidence
PM2.5, treated at high temperature and with a strong acid to hydrolyze any protein content and remove trace elements, was administered to BALB/c mice.
Establishes the untreated-particle comparator arm that this record holds, against which the abstract's reported rise in lung 4-OH-2-nonenal in the treated group is read.
Lung 4-OH-2-nonenal - acid/heat-treated PM2.5
4-OH-2-nonenal measured in lung of mice given PM2.5 stripped of bound protein and acid-soluble trace elements. Increased relative to pure PM2.5. Removing the acid-soluble metals therefore did NOT reduce lung lipid peroxidation — it raised it, which argues the oxidative-stress arm of PM2.5 toxicity in this model is carried by the residual (C/Si/Cl-enriched) particle core rather than by the acid-soluble metal fraction.
Exposure conditions
| Condition | Agent | Concentration | Duration |
|---|---|---|---|
| Acid- and heat-treated PM2.5 administration (bound protein hydrolyzed, trace elements removed) EXPOSURE:ogino-treated-pm25 |
fine respirable suspended particulate matter ENVO:01000415 |
— | — |
Outputs
| Group | Output | Description |
|---|---|---|
| treated | Lung 4-OH-2-nonenal - treated PM2.5 group OX:ogino-4hne-treated-pm25-output · under EXPOSURE:ogino-treated-pm25 |
Evidence
4-OH-2-nonenal levels in the lung was increased.
States directly that lung 4-OH-2-nonenal rose. In the abstract this clause sits in the sentence opening "On the contrary," which contrasts these endpoints with the attenuated ones, so the increase belongs to the acid/heat-treated PM2.5 group this record holds.
Response comparisons
AHR, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals attenuated airway hyperresponsiveness. Direction reported in the abstract; no value or p-value available without the full text.
BALF eosinophil percentage, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals attenuated the BALF eosinophil percentage — the eosinophilic, allergic arm of the response depends on that fraction. Direction reported in the abstract; no percentages given.
BALF neutrophil percentage, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals INCREASED the BALF neutrophil percentage. Opposite direction to the eosinophil comparison: the response shifts from eosinophilic to neutrophilic rather than disappearing. Direction reported in the abstract; no percentages given.
Lung IL-13 mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals attenuated lung IL-13 mRNA. Direction reported in the abstract; no value given.
Lung CXCL3 mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals attenuated lung CXCL3 mRNA. Direction reported in the abstract; no value given.
Lung MIP2a mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals increased lung MIP2a (CXCL2) mRNA, tracking the neutrophil rise. Direction reported in the abstract; no value given.
Lung TLR4 mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals increased lung TLR4 mRNA. Direction reported in the abstract; no value given.
Lung EGFR mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals increased lung EGFR mRNA. Direction reported in the abstract; no value given.
Lung Nrf2 mRNA, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals increased lung Nrf2 mRNA. Direction reported in the abstract; no value given.
Lung 4-OH-2-nonenal, treated PM2.5 vs pure PM2.5
Removing PM2.5-bound protein and acid-soluble metals increased lung 4-OH-2-nonenal. Direction reported in the abstract; no value given.
Key-event relationships
Airway inflammation leads to decreased lung function
In this component-subtraction experiment airway hyperresponsiveness, BALF eosinophil percentage and peribronchial inflammation were all attenuated together by the same manipulation (removal of PM2.5-bound protein and acid-soluble metals), linking the inflammatory key event to the functional outcome.
The treatment of PM2.5 with a strong acid at a high temperature attenuated AHR, eosinophil percentage in BALF, mRNA levels of IL-13 and CXCL3 and peribronchial inflammation.
AHR (the functional outcome) is attenuated in the same sentence, by the same manipulation, as BALF eosinophilia, IL-13/CXCL3 mRNA and peribronchial inflammation (the inflammatory key event). Co-attenuation of the upstream and downstream measures under one intervention is the coherence this relationship rests on; the abstract does not test the edge directly, hence moderate rather than strong support.
Protocols
High-temperature strong-acid treatment of PM2.5
Component-subtraction preparation of the test particle. PM2.5 was treated at high temperature and with a strong acid in order to hydrolyze any protein content and remove trace elements. The abstract reports the treatment reduced PM2.5-bound proteins and the percentages of the trace elements in PM2.5 in the order Zn > Cu > Pb > P > S > Mn > Fe > Ca > Ni, while the percentage of C, Si and Cl increased. Specific temperature, acid identity, concentration and contact time are not given in the abstract.
Equipment: Cyclone PM2.5 collection system
Airway hyperresponsiveness measurement
Airway hyperresponsiveness (AHR) was evaluated in each of the three groups. The abstract names AHR as an endpoint but gives no instrument, bronchoconstrictor agent, dose series or reported metric.
Bronchoalveolar lavage fluid cell differential
Bronchoalveolar lavage fluid (BALF) cells were evaluated and reported as eosinophil and neutrophil percentages. The abstract gives no lavage volume, stain or counting method.
Cytokine, chemokine and mucus protein mRNA measurement in lung
mRNA of various cytokines (IL-4, IL-5, IL-13, eotaxin-1 and CXCL3) and mucus protein mRNA (MUC5ac and MUC5b) were evaluated; the results section additionally reports mRNA expression of MIP2a, EGFR, Nrf2 and TLR4. The abstract names no platform, reference gene or primers.
Lung histology for inflammatory cell infiltration
The filtration of inflammatory cells in the lung was evaluated; the results are reported as peribronchial inflammation. The abstract names no fixation, section thickness or stain.
4-OH-2-nonenal measurement in lung
4-OH-2-nonenal (4-hydroxy-2-nonenal, a lipid peroxidation marker) levels were measured in the lung. The abstract names no detection method.